ABIM Critical Care key terms

The plateau airway pressure minus positive end-expiratory pressure during controlled ventilation. It reflects the cyclic stretch applied to aerated lung and is associated with mortality in acute respiratory distress syndrome, with values above about 15 cm H2O considered injurious.

The airway pressure measured during an end-inspiratory pause, representing alveolar pressure when airflow is zero. Elevated values suggest overdistension or stiff lungs and guide safe limits for tidal volume and positive end-expiratory pressure settings.

Airway pressure maintained at end-expiration that keeps alveoli open, improves oxygenation, and reduces cyclic recruitment and derecruitment. Excessively high levels can impair venous return and cause barotrauma, so titration balances oxygenation against hemodynamic and lung injury effects.

A ventilation strategy using low tidal volumes (about 6 mL/kg predicted body weight) and limited plateau pressures to reduce ventilator-induced lung injury. It is the standard of care in acute respiratory distress syndrome and is often applied to other critically ill patients.

A transient increase in airway pressure intended to reopen collapsed alveoli, followed by appropriate positive end-expiratory pressure to keep them open. Benefits are uncertain and risks include hypotension and barotrauma, so it is used selectively rather than routinely.

Placing a patient face down to improve oxygenation and survival in moderate-to-severe acute respiratory distress syndrome. It reduces ventral lung compression and improves ventilation-perfusion matching; careful turning and pressure-injury prevention are required.

Incomplete exhalation causing progressive gas trapping and rising end-expiratory alveolar pressure, often from high respiratory rate, obstruction, or short expiratory time. It can cause hypotension and hyperinflation and is managed by lowering rate, prolonging expiration, and treating obstruction.

Progressive air trapping during mechanical ventilation or severe airflow obstruction that raises intrathoracic pressure, impairs venous return, and can precipitate hypotension or cardiac arrest. Recognition requires attention to expiratory flow limitation and adequate expiratory time.

The process of assessing readiness and removing ventilator support, typically using a spontaneous breathing trial and evaluation of airway protection. Daily sedation interruption and early mobilization shorten duration, while failed trials prompt investigation of reversible causes.

Need for reintubation or ventilatory support shortly after planned extubation, often due to airway edema, weak cough, excessive secretions, or cardiac dysfunction. It is associated with worse outcomes, so pre-extubation assessment of airway and secretion clearance matters.

Cyclic variation in systolic or pulse pressure during positive-pressure ventilation, reflecting volume responsiveness in a patient without spontaneous effort or arrhythmia. Large variation suggests fluid responsiveness, but validity requires controlled ventilation and adequate tidal volume.

A bedside maneuver that transiently shifts venous blood from the legs to the thorax to test fluid responsiveness, ideally assessed by cardiac output or pulse pressure change. It is reversible and does not require giving fluid, but interpretation needs accurate measurement.

Pressure measured in the vena cava or right atrium, influenced by volume, venous tone, and cardiac function. Trends may inform resuscitation, but absolute values poorly predict fluid responsiveness, so it should not be used alone to guide fluid therapy.

Shock caused by mechanical obstruction to filling or ejection, such as tension pneumothorax, cardiac tamponade, or massive pulmonary embolism. It requires rapid identification and a procedure or reperfusion rather than fluids alone.

An exaggerated inspiratory fall in systolic blood pressure, commonly seen in cardiac tamponade and severe obstructive lung disease. It reflects impaired ventricular filling with respiration and is measured by careful cuff or arterial tracing.

Shock from inadequate cardiac output despite adequate filling, often after myocardial infarction or decompensated heart failure. Management targets the cause, cautious volume, inotropes or vasopressors, and early revascularization when ischemia is present.

Oxygen saturation of pulmonary arterial blood, reflecting the balance between oxygen delivery and consumption. Low values suggest inadequate delivery or increased demand, while high values can occur in sepsis with impaired extraction or shunting.

Controlled cooling or maintenance of normothermia after cardiac arrest or in selected neurologic injury to limit secondary brain damage. It requires sedation, shivering control, and gradual rewarming with attention to electrolytes and hemodynamics.

Measurement of pressure within the cranial vault using ventricular, parenchymal, or other devices to guide therapy for raised intracranial pressure. Management includes head elevation, sedation, osmotherapy, and cerebrospinal fluid drainage, with attention to cerebral perfusion pressure.

Mean arterial pressure minus intracranial pressure, representing the driving pressure for cerebral blood flow. Targets are individualized, and both hypotension and excessive pressure can worsen brain injury.

A clinical diagnosis requiring irreversible coma, absent brainstem reflexes, and apnea despite adequate stimulation, with confounding factors excluded. Institutional protocols and sometimes ancillary testing support the determination before organ donation discussions.

Continuous seizures or repeated seizures without recovery of consciousness, requiring immediate benzodiazepines followed by antiseizure medication. Refractory cases need anesthetic infusions and continuous electroencephalographic monitoring.

Electrographic seizure activity without obvious motor manifestations, common in critically ill or comatose patients. Diagnosis requires electroencephalography, and treatment follows status epilepticus principles.

An acute fluctuating disturbance of attention and cognition common in critically ill patients, associated with longer stays and worse outcomes. Prevention emphasizes sleep, orientation, early mobility, and minimizing deliriogenic medications.

An abrupt decline in kidney function identified by rising creatinine or falling urine output. Management focuses on treating the cause, avoiding nephrotoxins, maintaining perfusion, and initiating dialysis for refractory complications.

Slow, continuous extracorporeal clearance of solutes and fluid used in hemodynamically unstable critically ill patients. It allows gradual fluid removal and metabolic control but requires anticoagulation and vigilant monitoring for complications.

The percentage of filtered sodium excreted in urine, calculated from serum and urine sodium and creatinine. Low values often suggest prerenal states, but diuretics and intrinsic kidney disease can make interpretation unreliable.

Acidosis with elevated unmeasured anions, commonly from lactic acidosis, ketones, renal failure, or toxins. The gap helps narrow the differential, and treatment targets the underlying cause rather than the number alone.

The difference between measured and calculated serum osmolality, suggesting unmeasured osmoles such as toxic alcohols. It supports diagnosis in suspected poisoning and guides antidote use while definitive testing is pending.

Life-threatening organ dysfunction caused by a dysregulated response to infection, identified by clinical deterioration and markers such as rising organ dysfunction scores. Prompt antibiotics, source control, and supportive care improve outcomes.

Sepsis with persistent hypotension requiring vasopressors and elevated lactate despite adequate fluid resuscitation. It carries high mortality and requires rapid antibiotics, source control, and careful hemodynamic support.

Procedures that remove or drain the anatomic origin of infection, such as abscess drainage or debridement of necrotic tissue. Antibiotics alone are often insufficient, and delay is associated with worse outcomes.

The decline in blood lactate over time during resuscitation, reflecting improved perfusion and metabolism. Failure to clear suggests ongoing hypoperfusion or source and is used to guide reassessment rather than a single target value.

A metabolic emergency of insulin deficiency with ketosis, acidosis, and volume depletion, often triggered by infection or nonadherence. Treatment requires fluids, insulin, potassium replacement, and treatment of the precipitant.

Severe hyperglycemia with marked hyperosmolality and dehydration but minimal ketosis. It occurs mainly in older patients with type 2 diabetes and requires cautious fluid and insulin therapy with monitoring for osmotic shifts.

Metabolic derangements, especially hypophosphatemia, hypokalemia, and hypomagnesemia, after reintroducing nutrition in malnourished patients. Risk assessment and gradual feeding with electrolyte replacement prevent dangerous complications.

Acute glucocorticoid deficiency causing hypotension, weakness, and electrolyte abnormalities, often precipitated by stress or infection. Treatment is immediate hydrocortisone with fluids and correction of hypoglycemia and hyperkalemia.

Delivery of nutrients into the gastrointestinal tract, preferred over parenteral nutrition when feasible because it preserves gut function and reduces infection risk. Monitoring includes tolerance, aspiration risk, and electrolyte shifts.

Bleeding proximal to the ligament of Treitz, often from ulcers or varices, presenting with hematemesis or melena. Management includes resuscitation, acid suppression, and urgent endoscopy, with variceal bleeding requiring specific therapy.

Reversible neuropsychiatric dysfunction from liver failure and portosystemic shunting, often precipitated by infection, bleeding, or electrolyte disturbance. Treatment includes lactulose and rifaximin plus correction of precipitants.

Infection of ascitic fluid in cirrhosis without an obvious surgical source, diagnosed by elevated ascitic neutrophil count. Prompt antibiotics and albumin reduce mortality, and recurrence is prevented with prophylaxis.

Systemic activation of coagulation with consumption of platelets and clotting factors, causing bleeding and thrombosis. Treatment targets the underlying cause, with blood products guided by bleeding rather than laboratory values alone.

Sustained intra-abdominal hypertension causing organ dysfunction, particularly respiratory and renal impairment. It is managed by decompression, including medical measures and sometimes laparotomy.

A strategy for major trauma emphasizing hemorrhage control, balanced blood product transfusion, permissive hypotension, and prevention of hypothermia and acidosis. It prioritizes physiology over definitive repair until stability improves.

A structured system for rapidly delivering balanced blood products and adjuncts in severe hemorrhage. It reduces delays and improves coordination while monitoring calcium, temperature, and coagulation.

Fluid replacement in major burns guided by urine output and hemodynamics, often starting with weight- and burn-size-based formulas. Over-resuscitation causes edema and compartment syndromes, so titration matters.

A recognizable constellation of signs and symptoms suggesting a class of poisoning, such as anticholinergic, opioid, or sympathomimetic patterns. It guides empiric antidote use and supportive care before confirmatory testing.

An opioid receptor antagonist used to reverse opioid-induced respiratory depression and coma. Because its duration may be shorter than the opioid, monitoring and repeat dosing or infusion are needed.

A potentially fatal condition from serotonergic excess causing agitation, clonus, hyperreflexia, and hyperthermia. Treatment includes stopping offending agents, supportive care, and sometimes cyproheptadine.

Delivery of an unsynchronized high-energy shock to terminate ventricular fibrillation or pulseless ventricular tachycardia. Early defibrillation is a key determinant of survival in cardiac arrest.

The effectiveness of chest compressions and ventilations during arrest, including rate, depth, recoil, and minimal interruptions. High-quality technique improves the likelihood of return of spontaneous circulation.

Organized supportive care after return of spontaneous circulation, including oxygenation and ventilation targets, hemodynamic support, neurologic prognostication, and temperature control. It reduces secondary injury and guides family communication.

Permission for treatment obtained after explaining risks, benefits, and alternatives, with exceptions when immediate care is needed to prevent serious harm. When the patient lacks capacity, surrogate decision-making or emergency provisions apply.

Decisions made by a designated person on behalf of a patient lacking capacity, ideally using the patient's known values and preferences. When preferences are unknown, the standard shifts to the patient's best interests.

A conversation aligning treatment with the patient's values, prognosis, and priorities, often clarifying code status and limits. It should be documented and revisited as the clinical situation changes.

Interdisciplinary care addressing symptoms, psychosocial needs, and quality of life for patients with serious illness, appropriate alongside curative treatment. It differs from hospice in eligibility and intent.

A bloodstream infection attributed to a central venous catheter, reduced by insertion bundles, site selection, and prompt removal of unnecessary lines. Surveillance and reporting support quality improvement.

Pneumonia developing after at least 48 hours of mechanical ventilation, often from microaspiration. Prevention includes head elevation, sedation minimization, and oral care, while diagnosis requires clinical and microbiologic correlation.

Periodic reduction or pause of sedative infusions to assess neurologic status and reduce oversedation. It shortens ventilation and intensive care stays but requires monitoring for agitation and withdrawal.

A structured method to identify underlying system failures contributing to an adverse event and to design preventive changes. It complements, but does not replace, disclosure and support for affected patients and staff.