Free PCCN (Adult) Exam Flashcards

NSTEMI can produce ischemic ST depression, T-wave changes, or even an initially nondiagnostic ECG. Continue serial ECG and troponin assessment when symptoms suggest acute coronary syndrome; do not use one normal-looking tracing to dismiss evolving ischemia.

Hypotension with jugular venous distention and relatively clear lungs suggests impaired right-ventricular output. Escalate promptly and avoid casually reducing preload, because venodilation or over-diuresis can worsen hypotension.

Increasing dyspnea or orthopnea accompanied by rising weight, crackles, edema, or greater oxygen need points to fluid accumulation. A trend across symptoms, weight, intake/output, and examination is more useful than one isolated value.

Use synchronized cardioversion when the tachyarrhythmia is causing hemodynamic instability, ongoing ischemia, acute heart failure, shock, or altered mentation. Synchronization avoids delivering the shock during the vulnerable repolarization period.

Pulseless ventricular tachycardia is a cardiac-arrest rhythm requiring CPR and unsynchronized defibrillation. Unstable monomorphic VT with a pulse is treated with synchronized cardioversion when synchronization can be achieved.

It signals increased risk for torsades de pointes, especially with bradycardia, low potassium or magnesium, or QT-prolonging drugs. Review medications and electrolytes, monitor the rhythm closely, and escalate a worsening trend.

Hypotension, rising jugular venous pressure, muffled heart sounds, pulsus paradoxus, or narrowing pulse pressure suggest impaired filling and obstructive shock. This is an urgent deterioration requiring rapid evaluation and possible pericardial drainage.

New back, flank, abdominal, or groin pain with hypotension, tachycardia, pallor, or falling hemoglobin can indicate concealed bleeding even when the puncture site looks dry. Keep the patient supine as appropriate and escalate immediately.

That level approximates the right atrium and provides the reference for pressure measurement. A transducer below the reference reads falsely high; one above reads falsely low. Relevel after position changes before treating an unexpected value.

Failure to capture shows a pacing spike not followed by the expected atrial or ventricular response. Failure to sense means the pacemaker misses intrinsic activity and fires inappropriately. Both require patient assessment first and prompt device evaluation.

Pulse oximetry reflects oxygenation, not carbon-dioxide clearance. Supplemental oxygen may preserve SpO2 while ventilation deteriorates, so trend respiratory effort, mental status, capnography, and blood gases when hypoventilation is possible.

The pH falls while PaCO2 rises, showing inadequate alveolar ventilation. Bicarbonate may be near normal early or elevated with renal compensation in a chronic process; compare the pattern with the patient's baseline and clinical status.

It suggests worsening hypoventilation and carbon-dioxide retention. Assess airway, sedation or opioid effect, respiratory effort, and level of consciousness immediately rather than waiting for oxygen saturation to fall.

Intermittent bubbling with cough or exhalation may reflect air leaving the pleural space. Continuous bubbling suggests an air leak and should trigger a system-to-patient check; do not clamp routinely because trapped air can create tension physiology.

Sudden respiratory distress with unilateral absent breath sounds plus hypotension, tachycardia, distended neck veins, or rapidly rising airway pressures suggests obstructive shock from trapped pleural air. Do not delay emergency decompression for a routine chest x-ray.

Abrupt unexplained dyspnea, pleuritic chest pain, tachycardia, syncope, hypoxemia, or new right-heart strain should prompt urgent evaluation. A relatively unremarkable lung examination does not exclude pulmonary vascular obstruction.

It is unsafe when the patient cannot protect the airway, cannot clear secretions, is vomiting, is severely unstable, or is failing despite support. Worsening mental status, gas exchange, or work of breathing calls for immediate escalation toward a definitive airway.

DKA is defined by significant ketone production and metabolic acidosis. HHS is dominated by severe hyperglycemia, hyperosmolality, and dehydration with little or no major ketoacidosis; overlap can occur, so assess ketones, pH, bicarbonate, and osmolality together.

Insulin deficiency and acidosis shift potassium out of cells while osmotic diuresis removes it from the body. Insulin and volume treatment drive serum potassium down, so frequent monitoring and protocol-based replacement are essential; markedly low potassium must be corrected before insulin proceeds.

SIADH retains water, producing low-volume concentrated urine and dilutional hyponatremia. Diabetes insipidus loses free water, producing high-volume dilute urine with risk of hypernatremia and dehydration.

A substantial platelet fall, often about 50% from baseline several days after heparin exposure, is more concerning than the absolute count alone—especially with new thrombosis. Stop all heparin sources, notify the team, and anticipate non-heparin anticoagulation after evaluation.

Determine the last-known-well time, not merely when symptoms were discovered. It anchors reperfusion eligibility; simultaneously activate the stroke pathway, check glucose, perform a focused neurologic assessment, and obtain urgent brain imaging.

Stroke can impair swallowing without obvious choking, creating aspiration risk. Keep food, fluids, and oral medications withheld until an approved screen is passed or a specialist establishes a safe plan.

Delirium has an acute, fluctuating course with impaired attention and altered awareness. Dementia is usually gradual and more stable across a day; a sudden change in a patient with dementia should still be treated as possible delirium and investigated for a reversible cause.

Widening pulse pressure, bradycardia, and irregular respirations are late signs of dangerously increased intracranial pressure and possible herniation. Protect the airway, keep head and neck aligned as appropriate, and activate emergency escalation.

Yes. Bright red or maroon stool usually suggests a lower source, but a brisk upper GI hemorrhage can move rapidly enough to cause hematochezia. Hemodynamic instability matters more than stool color when setting urgency.

New confusion, sleep-pattern reversal, reduced attention, or asterixis can signal encephalopathy. Look for triggers such as GI bleeding, infection, constipation, dehydration, renal dysfunction, or sedatives; the clinical trend matters more than an ammonia value alone.

When tolerated, early oral or enteral nutrition helps maintain gut integrity and is generally preferred to unnecessary prolonged NPO status or parenteral nutrition. Feeding route and timing still depend on severity, ileus, aspiration risk, and the prescribed plan.

Severe pain out of proportion to the initial abdominal examination is a classic warning, especially with embolic risk or low-flow shock. Peritoneal signs can appear late; urgent vascular or surgical evaluation should not wait for them.

Falling urine output with volume loss or poor perfusion, orthostasis, tachycardia, or hypotension supports reduced renal blood flow. Review intake/output, weight, nephrotoxins, and hemodynamics; failure to improve after the cause is corrected suggests intrinsic or obstructive injury.

Calcium rapidly reduces the heart's immediate electrical risk but does not remove potassium or meaningfully lower its serum concentration. Separate measures must shift potassium into cells and remove it from the body while ECG and potassium are reassessed.

Pain out of proportion to the injury—especially pain worsened by passive stretch—plus a tense compartment or sensory change is concerning. A palpable pulse does not rule it out because pulselessness is late; remove external constriction and seek urgent surgical evaluation.

Suspected infection plus new organ dysfunction or hypoperfusion—such as altered mentation, hypotension, rising oxygen need, oliguria, or elevated lactate—requires prompt action. Obtain ordered cultures without delaying antimicrobials and trend response to resuscitation.

Early distributive shock may show warm skin, bounding pulses, and low vascular resistance despite hypotension. Hypovolemic shock more often causes cool clammy skin and vasoconstriction; neither pattern is absolute, so use perfusion trends and the clinical cause.

Intramuscular epinephrine in the anterolateral thigh is first line. Oxygen, fluids, bronchodilators, antihistamines, and corticosteroids may support care, but they do not replace epinephrine or repeated airway and hemodynamic assessment.

An unstageable injury has full-thickness loss whose depth is obscured by slough or eschar. Deep-tissue pressure injury presents as persistent deep red, maroon, or purple discoloration or a blood-filled blister from underlying damage; do not relabel either as a numbered stage without meeting its definition.

Ask whether each urinary catheter and central line is still necessary. Use aseptic insertion and maintenance, preserve closed systems and intact dressings, and promptly remove devices that no longer have a valid indication rather than replacing them routinely by calendar.

Muscle breakdown releases myoglobin and electrolytes, creating risk for acute kidney injury, hyperkalemia, hypocalcemia early in the course, and dysrhythmias. Trend urine output, renal function, creatine kinase, potassium, and volume status during prescribed fluid therapy.

Support ventilation and the airway immediately while administering naloxone per protocol. Naloxone may wear off before the opioid, so reassess continuously, repeat treatment when indicated, and watch for recurrent respiratory depression or acute withdrawal.

Alcohol withdrawal can progress to seizures, delirium tremens, severe autonomic instability, and death. Opioid withdrawal is often intensely distressing but is less often directly fatal; use the appropriate tool—such as CIWA-Ar or COWS—and escalate based on the syndrome and patient risk.

Assess decision-making capacity for the specific choice: can the patient understand relevant information, appreciate consequences, reason about options, and communicate a choice? Capacity can fluctuate and is not lost merely because the decision seems unwise.

A capable patient's current decision governs; if capacity is absent, follow the valid advance directive and authorized surrogate using substituted judgment or best interests. Escalate unresolved conflict through the clinical and ethics channels rather than letting the loudest voice decide.

Verify identity, voluntariness, apparent capacity, and that the signature is properly witnessed. The clinician performing the procedure is responsible for explaining material risks, benefits, and alternatives; pause and contact that clinician if the patient still has unanswered questions.

A qualified interpreter improves accuracy, confidentiality, and informed participation while reducing omission and coercion risk. Speak directly to the patient, use plain language, and reserve family interpretation for true emergencies or the patient's informed preference under policy.

Teach-back asks the patient or caregiver to explain the plan in their own words or demonstrate the skill. It tests how clearly the team taught—not the patient's intelligence—and reveals gaps that a yes/no question commonly misses.

Palliative care addresses symptoms, communication, and quality of life at any serious-illness stage and can accompany disease-directed treatment. Hospice is a specific end-of-life care model tied to eligibility and a comfort-focused plan; referral to palliative care does not mean giving up treatment.

State the immediate situation, relevant background, your focused assessment, and a clear recommendation or request. Close the loop by reading back critical orders and confirming who will do what by when.

Activate it for acute deterioration or serious concern that needs resources beyond the unit response—even before a single vital sign crosses a threshold. Use trend recognition, bedside concern, and the chain of escalation; do not delay because the primary team has not yet responded.

PDSA tests a change on a small scale: plan the intervention and measure, do the test, study results against the prediction, then adopt, adapt, or abandon the change. It is iterative learning, not proof from one successful trial.

Optimal outcomes occur when nurse competencies are matched to the patient's and family's characteristics and needs. As vulnerability, complexity, or unpredictability rises, the required level of clinical judgment, advocacy, collaboration, and systems thinking also changes.