Free CCRN (Adult) Exam Flashcards

Low PA wedge pressure and CVP with low cardiac index and a compensatory high SVR. The pump and vasculature are intact and the deficit is volume, so fluid resuscitation is the first priority rather than vasopressors or inotropes.

High PA wedge pressure and CVP with low cardiac index and high SVR. The pump has failed, so fluid will worsen pulmonary edema; therapy targets the failing heart with inotropes, vasopressors, and mechanical support such as IABP or Impella.

Low SVR with normal or high cardiac index and warm extremities; PA wedge pressure is variable. Vasodilation dominates, so treatment combines fluids, vasopressors (norepinephrine first), and source control rather than fluid alone.

Mechanical impedance to forward flow: cardiac tamponade, tension pneumothorax, and massive pulmonary embolism. Hallmarks include equalization of diastolic pressures (tamponade) or low PA wedge with high SVR (PE or pneumothorax); fix the obstruction, not just the blood pressure.

Reflects left atrial and left ventricular end-diastolic pressure when the catheter tip is wedged. Used to separate cardiogenic pulmonary edema (high PAWP) from non-cardiogenic causes such as ARDS (normal or low PAWP).

Cardiac output is total L/min pumped; cardiac index divides it by body surface area (L/min/m2). CI removes body-size bias and is the value shock definitions and treatment goals use, with a CI below 2.2 suggesting a failing or underfilled pump.

Afterload marker calculated from MAP, CVP, and cardiac output. High SVR indicates compensatory vasoconstriction in low-output states; low SVR indicates pathologic vasodilation typical of distributive shock and guides vasopressor selection.

Inflates during diastole to raise coronary perfusion and deflates at systole to drop afterload. Contraindicated in aortic insufficiency because diastolic inflation would worsen regurgitant flow back into the left ventricle.

Mild P/F 200-300, moderate 100-200, severe 100 or less, all with PEEP at least 5 cmH2O. Severity drives ventilation strategy: severe ARDS needs low tidal volume, prone positioning, and judicious PEEP titration, not simply more oxygen.

Oxygenation failure is low PaO2 from V/Q mismatch, shunt, or diffusion impairment; ventilation failure is high PaCO2 from alveolar hypoventilation or increased dead space. The first raises FiO2 and PEEP, the second raises minute ventilation.

A bedside index of gas exchange that does not require a PA catheter. Lower values mean worse oxygenation per unit of inspired oxygen and anchor the Berlin ARDS severity criteria.

Tidal volume 6 mL/kg predicted body weight, plateau pressure below 30 cmH2O, and permissive hypercapnia. Smaller tidal volumes lower mortality by reducing ventilator-induced lung injury from cyclic overdistention.

Keeps alveoli open at end-expiration, recruits lung, and improves oxygenation. Too much PEEP can drop venous return and cardiac output and raise intrathoracic pressure, so oxygenation gains must be weighed against perfusion losses.

Rising PaCO2 from hypoventilation produces respiratory acidosis; falling PaCO2 from hyperventilation produces respiratory alkalosis. The lungs drive CO2 and the kidneys compensate slowly, so acute changes show before metabolic compensation appears.

Trapped gas in obstructive disease (COPD or asthma) raises end-expiratory alveolar pressure above set PEEP. It can cause hypotension from reduced venous return and breath stacking; manage by lowering rate or tidal volume and giving bronchodilation.

Total-body potassium is depleted even when serum potassium reads normal or high, because acidosis shifts K+ extracellularly. Insulin reverses that shift, so hold insulin and replace K+ first when serum K+ is below 3.3 mEq/L to prevent life-threatening hypokalemia and arrhythmia.

DKA shows metabolic acidosis (pH below 7.3, bicarbonate below 18) with ketones; HHS shows extreme hyperglycemia and hyperosmolality without ketoacidosis. Both need fluids and insulin, but DKA requires closer potassium and acidosis management.

Storm is hyperadrenergic with fever, tachycardia, agitation, and arrhythmia; treat with beta-blocker, thionamide, iodine, and steroids. Myxedema coma is severe hypothyroidism with hypothermia, hypoventilation, hyponatremia, and mental slowing; treat with IV levothyroxine and hydrocortisone.

Glucocorticoid deficiency under physiologic stress presents as refractory hypotension with hyponatremia and hyperkalemia in primary disease. Empiric IV hydrocortisone in vasopressor-dependent septic shock can stabilize hemodynamics while the cause is evaluated.

Simultaneous microvascular clotting and consumption of platelets and clotting factors, so the patient both thromboses and bleeds. Treatment is the underlying trigger plus factor and platelet support for bleeding; anticoagulation alone is not the answer.

Immune-mediated platelet fall of 50 percent or more, typically 5-10 days after heparin start. Stop ALL heparin (including line flushes) and switch to a direct thrombin inhibitor such as argatroban or bivalirudin; do not give platelet transfusions.

Fever with absolute neutrophil count below 500 (or below 1000 with a predicted drop) is a medical emergency. Empiric broad-spectrum antibiotics within one hour, before source workup completes, because untreated bacteremia is rapidly fatal in this group.

Functional renal failure in advanced cirrhosis without intrinsic kidney disease; splanchnic vasodilation drops effective arterial volume and triggers renal vasoconstriction. Albumin plus a vasoconstrictor (terlipressin or octreotide) is the directed therapy, not fluid alone.

Ascitic fluid with neutrophil count 250/mm3 or more in a cirrhotic patient. Empiric third-generation cephalosporin (cefotaxime) plus albumin lowers progression to hepatorenal syndrome and mortality.

Combine early endoscopic band ligation with a vasoactive drug (octreotide or terlipressin) to drop portal pressure and prophylactic antibiotics to prevent SBP. Airway protection and resuscitation precede endoscopy in unstable patients.

Pre-renal is volume or perfusion responsive (BUN:Cr above 20, bland sediment); intrinsic is tubular, interstitial, or glomerular (ATN with muddy brown casts); post-renal is obstruction. The category changes strategy: give volume for pre-renal, remove nephrotoxins in intrinsic, relieve obstruction in post-renal.

CRRT runs continuously with slow solute and fluid clearance and is preferred when hemodynamics cannot tolerate rapid shifts. Intermittent HD delivers rapid clearance but pulls volume fast, suited to stable ICU patients.

CPP = MAP minus ICP. Brain Trauma Foundation guidance targets 60-70 mmHg in severe TBI; CPP too low causes ischemia, and CPP too high can worsen cerebral edema by raising capillary hydrostatic pressure.

Sustained ICP above 22 mmHg in severe TBI warrants intervention because herniation and ischemia risk rise. First-tier therapy is head elevation, sedation, normoxia, and normocapnia, then osmotic therapy (hypertonic saline or mannitol) for refractory cases.

Ipsilateral pupil dilation from CN III compression and contralateral hemiparesis from cerebral peduncle compression. This is an emergency: secure the airway, use mild hyperventilation as a temporizing measure, give osmotic therapy, and obtain immediate neurosurgical evaluation.

Brain death is irreversible loss of all brain and brainstem function (no reflexes, no apnea) and legally equals death. Vegetative state preserves brainstem reflexes and spontaneous breathing, so the patient is alive but unconscious; the distinction drives organ donation and withdrawal decisions.

Guideline-supported within 3 hours of symptom onset, extended to 4.5 hours in selected patients. Door-to-needle time matters; eligibility hinges on bleeding-risk exclusions and a non-hemorrhagic CT first.

Start antibiotics within one hour of suspicion; draw blood cultures first when safe but do not delay antibiotics for LP or imaging if there will be a delay. Add dexamethasone for suspected pneumococcal meningitis to reduce neurologic sequelae.

Acute, fluctuating attention and cognition in ICU, assessed with the CAM-ICU tool. Linked to longer ventilation, longer stay, and higher mortality; reduce modifiable drivers (sedation depth, sleep disruption, immobility, infection) before adding antipsychotics.

Least restrictive, time-limited, with documented indication and reassessment. Physical restraints can worsen delirium and injury risk; non-pharmacologic de-escalation and family presence are preferred, and restraints are a last resort for imminent danger, not for convenience.

Life-threatening organ dysfunction caused by a dysregulated host response to infection. Operationally identified by an acute SOFA rise of 2 or more points from baseline; qSOFA (altered mentation, SBP 100 or less, RR 22 or higher) is a bedside screen to suspect sepsis, not a diagnostic criterion.

Sepsis requiring vasopressors to hold MAP at 65 mmHg or higher AND serum lactate above 2 mmol/L despite adequate fluid resuscitation. Both criteria together signal circulatory and cellular or metabolic failure.

Sequential or simultaneous failure of two or more organs unresponsive to resuscitation. It is the downstream consequence of uncontrolled sepsis or SIRS; management is source control plus individualized organ support, not a single therapy.

Start with roughly 30 mL/kg crystalloid and reassess with lactate, MAP, and urine output. Patients who remain hypotensive despite fluid need vasopressors; further blanket fluids without responsiveness can worsen pulmonary edema.

Norepinephrine. Alpha-mediated vasoconstriction with modest beta support raises MAP without the tachyarrhythmia burden of epinephrine or dopamine. Add vasopressin rather than escalating norepinephrine alone.

Trending lactate over time assesses resuscitation adequacy; failure to clear (less than 10 percent reduction over 2-6 hours) signals ongoing hypoperfusion and worse outcomes. Capillary refill time and mottling are bedside complements.

Maintain perfusion, normothermia, and normoglycemia; manage diabetes insipidus with desmopressin or vasopressin; some programs add hormone replacement (thyroid, cortisol, vasopressin) to stabilize hemodynamics and preserve organ viability for transplantation.

Patient characteristics drive the nurse competencies required; when nurse competencies match patient needs, synergy produces optimal outcomes. Patient characteristics include resiliency, vulnerability, stability, complexity, predictability, and participation; competencies include clinical judgment, advocacy, and collaboration.

Acting or speaking on behalf of the patient and family when they cannot: protecting autonomy, ensuring informed consent, navigating conflicts, and escalating goals-of-care mismatches. Advocacy is a Synergy Model competency, not just a personal trait.

Clinicians and the patient or surrogate exchange information about options, prognosis, and patient values, then agree on a plan. Contrast with paternalism (clinician decides alone) and uninformed choice (information dumped without guidance).

Autonomy respects the patient's right to choose; beneficence promotes good; non-maleficence avoids harm; justice distributes benefits and burdens fairly. ICU conflicts usually pit autonomy against beneficence or non-maleficence at end of life.

Capacity, disclosure of risks/benefits/alternatives, understanding, voluntariness (no coercion), and consent. If the patient lacks capacity, the surrogate or legally authorized representative decides using substituted judgment or best-interest standards.

Aligns treatment intensity with patient values and prognosis; may shift from curative to palliative or limit life support. Revisit as the clinical trajectory changes and document outcomes so the whole team carries the same plan.

Symptom-focused care that supports patients and families regardless of prognosis; it can coexist with curative treatment and is not only end-of-life care. Early palliative consults reduce non-beneficial treatment and improve family satisfaction.

Knowing the ethically correct action but being constrained from acting, common when non-beneficial treatment continues. Manifests as frustration, burnout, and withdrawal; address via ethics consult, communication structures, and institutional support, not just individual resilience.