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NURS 251 Final Exam – Critical Care Section (Latest 2026/2027 Update) | Complete Q&A with Verified Answers & Detailed Rationales | Respiratory Failure, Mechanical Ventilation, ABG Interpretation, ARDS | A+ Grade | Penn State University

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INSTANT PDF DOWNLOAD - This is the comprehensive Critical Care Section study guide for the NURS 251 Final Exam at Penn State University (Latest 2026/2027 Update), featuring verified exam questions with correct answers and detailed rationales. Covers oxygenation failure (Type 1: PaO2 60 mmHg, SaO2 90%; Type 2: PaCO2 45 with pH 7.35), mechanical ventilation (FiO2, PEEP, tidal volume, weaning parameters, alarms, VAP prevention), ABG interpretation (normal ranges: pH 7.35-7.45, PaCO2 35-45, HCO3 22-26), uncompensated/partially/fully compensated disorders, ARDS pathophysiology and prone positioning, chest trauma (pneumothorax, hemothorax, flail chest), FAST exam, ABCDE trauma algorithm, and ICU complications (VAP, DVT, stress ulcers, sedation management, nutrition) . Aligned with Penn State NURS 251 curriculum and NCLEX-RN standards. INSTANT DIGITAL DOWNLOAD (PDF) immediately upon purchase. Fully text-searchable, printable, and accessible anytime. Trusted by Penn State nursing students for exam success. 100% satisfaction guarantee. NURS 251 Final Exam PSU Critical Care Nursing Penn State Nursing Respiratory Failure Type 1 Oxygenation Failure Type 2 Ventilatory Failure PaO2 60 mm Hg SaO2 Less Than 90 Mechanical Ventilation FiO2 Settings PEEP Positive End Expiratory Pressure Ventilator Alarms VAP Prevention ABG Interpretation pH Normal Range 7.35 7.45 PaCO2 Normal 35 45 HCO3 Normal 22 26 Respiratory Acidosis Respiratory Alkalosis Uncompensated ABG Partially Compensated ABG ARDS Pathophysiology Prone Positioning ARDS Chest Trauma Nursing Pneumothorax Hemothorax Flail Chest Paradoxical Movement ABCDE Trauma Algorithm FAST Exam Trauma ICU Complications DVT Prophylaxis Stress Ulcer Prevention Sedation Management ICU Ventilator Weaning Nursing Midterm Exam PSU NCLEX Critical Care Prep A+ Grade Study Guide

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NURS 251 — Final Examination (Critical Care Section)
T R A U M AT I C B R A I N I N J U R Y, S P I N A L CO R D I N J U R Y & I N T R A C R A N I A L P R E SS U R E M A N A G E M E N T

INSTITUTION Penn State University — College of COURSE CODE NURS 251
Nursing
PROGRAM Bachelor of Science in Nursing (BSN) ACADEMIC YEAR
EXAM TITLE Final Exam — Critical Care Section (TBI, TOTAL QUESTIONS 75 Questions
SCI, ICP)
ACCREDITATION MSCHE — Middle States Commission on FORMAT Multiple Choice — Select the Single Best
Higher Education Answer


EXAMINATION INSTRUCTIONS
▸ Select the single best answer for each question based on NURS 251 critical care content.
▸ Questions cover traumatic brain injury (epidural/subdural hematoma, concussion, diffuse axonal injury), intracranial pressure
(ICP) and cerebral perfusion pressure (CPP) management, spinal cord injury (SCI) syndromes and complications, and neuro
assessment.
▸ Glasgow Coma Scale scoring, Cushing's Triad, Monro-Kellie doctrine, CPP calculation, and autonomic dysreflexia recognition
are essential.
▸ Correct answers and clinical rationales appear below each question for examination review.
▸ All content aligns with Penn State University BSN curriculum and MSCHE accreditation standards.


SECTION I — TRAUMATIC BRAIN INJURY, ICP, CPP & SPINAL CORD Questions 1 –
INJURY 75

1. What are the two major mechanisms of injury in traumatic brain injury (TBI)?
A. Ischemic and hemorrhagic
B. Blunt (falls, MVC, sports, assault) and Penetrating (firearms, objects through skull into brain)
C. Primary and Secondary
D. Diffuse and Focal
CORRECT ANSWER B — Blunt (falls, MVC, sports injuries, assault) and Penetrating (inserted through the skull & possibly
into the brain — unintentional injuries/firearms)
RATIONALE Mechanism of injury describes HOW the trauma occurred, which guides assessment and anticipated injuries.
Blunt trauma (most common) transfers energy through the skull without penetration —
acceleration/deceleration and rotational forces cause brain injury. Penetrating trauma breaches the skull and
dura, introducing infection risk and causing direct tissue destruction along the projectile path. Knowing the
mechanism helps the nurse anticipate associated injuries: blunt trauma → cervical spine injury, facial
fractures; penetrating trauma → open fractures, CSF leak, infection risk.

, 2. What concurrent injuries must be considered with traumatic brain injury?
A. Only extremity fractures
B. Cervical spine injuries (require C-collar and safe movement), vertebral column injuries, and facial fractures (airway
and eye concerns)
C. Only internal organ injuries
D. Only pelvic fractures
CORRECT ANSWER B — Cervical spine injuries (need safe movement/C-collar), vertebral column injuries (down the spine),
and facial fractures (airway issues from swelling/blood and eye issues)
RATIONALE TBI patients have a high incidence of concurrent cervical spine injury (5–10%) because the same force that
injured the brain also stresses the neck. The cervical spine must be presumed injured until cleared by imaging
— maintaining C-collar and spinal precautions. Facial fractures threaten the airway (edema, bleeding,
displaced structures) and can cause vision-threatening injuries (orbital fractures, optic nerve damage).
Vertebral column injuries may occur anywhere along the spine. These concurrent injuries directly impact
airway management, positioning, and surgical priorities.


3. What is a primary brain injury?
A. Damage caused by pathophysiologic changes after the initial injury
B. Direct transfer of energy leading to injury at the moment of impact — fractures and bleeds from head hitting
something and brain hitting skull
C. Injury from hypotension and hypoxia
D. Cerebral edema that develops days later
CORRECT ANSWER B — Direct transfer of energy leading to injury at the moment of impact — fractures, bleeds from head
hitting something, brain hitting skull
RATIONALE Primary injury is the irreversible mechanical damage occurring at the moment of trauma: skull fractures,
cerebral contusions, lacerations of brain tissue, shearing of axons, and disruption of blood vessels causing
hemorrhage. Neuronal destruction from primary injury is PERMANENT — neurons do not regenerate. The
clinical goal is to prevent secondary injury, which is potentially preventable and treatable. Primary injury
severity determines the baseline neurological deficit; secondary injury determines whether the patient
deteriorates from that baseline.


4. What is secondary brain injury and what causes it?
A. Direct mechanical damage at the moment of impact
B. Injury caused by pathophysiologic changes after the primary injury — hypotension (low blood supply to brain),
hyperthermia, hypoxia, cerebral edema, and increased ICP
C. A second impact occurring days after the first
D. Injury limited to the skull only
CORRECT ANSWER B — Caused by pathophysiologic changes after primary injury: hypotension, hyperthermia, hypoxia,
cerebral edema, and increased ICP — these changes further damage vulnerable cells
RATIONALE Secondary injury is the "insult after the insult" — potentially PREVENTABLE and TREATABLE brain damage
occurring minutes to days after the primary injury. Key mechanisms: hypotension (SBP <90 mmHg →
decreased cerebral perfusion → ischemia), hypoxia (PaO2 <60 mmHg → anaerobic metabolism → cell death),
hyperthermia (increases cerebral metabolic rate → increased oxygen demand), cerebral edema (increases ICP
→ decreases perfusion), and elevated ICP (>20 mmHg → brain herniation). The ischemic penumbra
(surrounding tissue at risk) may die or survive depending on secondary injury prevention. THIS IS THE
NURSE'S PRIMARY FOCUS — preventing secondary injury through meticulous hemodynamic, respiratory, and
ICP management.

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