ABPS Hospital Medicine key terms

Life-threatening organ dysfunction caused by a dysregulated host response to infection, identified clinically by an acute rise in the SOFA score of at least two points. It replaced earlier criteria requiring systemic inflammatory response signs.

Sepsis with persisting hypotension requiring vasopressors to maintain mean arterial pressure of at least 65 mmHg plus a serum lactate above 2 mmol/L despite adequate fluid resuscitation. Mortality is substantially higher than in sepsis alone.

Bedside screen scoring one point each for respiratory rate of 22 or more, altered mentation, and systolic blood pressure of 100 mmHg or less. Two or more points flag patients at higher risk of poor outcome but it is not a stand-alone diagnostic test.

Sequential Organ Failure Assessment: a points system grading respiratory, coagulation, hepatic, cardiovascular, neurologic, and renal dysfunction. Higher totals indicate worse organ failure and predict mortality in critically ill patients.

The decline in serum lactate over time during resuscitation, commonly expressed as a percentage of the initial value. Failure to clear lactate suggests ongoing hypoperfusion or inadequate source control.

Practice of starting norepinephrine as the initial vasopressor in septic shock, often through a peripheral line while central access is arranged. Early use reduces fluid overload and shortens time to target mean arterial pressure.

Adding vasopressin to norepinephrine in septic shock, typically when norepinephrine requirements escalate, to reduce catecholamine dose and support blood pressure through a non-adrenergic receptor pathway.

Acute onset within one week of a known insult, bilateral opacities not fully explained by effusion or collapse, hypoxemia with P/F ratio of 300 or less on positive pressure, and respiratory failure not primarily cardiogenic. Severity is graded by P/F ratio.

Ventilator strategy using low tidal volumes of roughly 6 mL/kg predicted body weight and plateau pressures of 30 cm H2O or less. It reduces ventilator-induced lung injury and mortality in acute respiratory distress syndrome.

Plateau pressure minus applied positive end-expiratory pressure. It reflects the cyclic stretch delivered to aerated lung and higher values are associated with increased mortality in ARDS.

Placing a hypoxemic patient face down for prolonged sessions, typically 12 to 16 hours daily. In moderate-to-severe ARDS it improves oxygenation and reduces mortality by recruiting dorsal lung and homogenizing stress.

Air trapping in which end-expiratory alveolar pressure exceeds the set extrinsic PEEP, usually from incomplete exhalation in obstructive disease or high minute ventilation. It causes dynamic hyperinflation, hypotension, and misinterpreted plateau pressures.

Deliberate acceptance of elevated carbon dioxide with pH above roughly 7.20 to protect the lung from injurious tidal volumes or to limit breath stacking. It is used in ARDS and severe obstructive exacerbations.

A transient increase in airway pressure intended to reopen collapsed alveoli, followed by adequate PEEP to keep them open. Evidence for routine use is weak and it can cause hypotension or barotrauma.

Myocardial injury with rising troponin due to acute plaque rupture or erosion with thrombus, causing coronary occlusion and ischemia. Management centers on reperfusion and secondary prevention.

Myocardial injury with ischemia caused by a supply-demand mismatch, such as sepsis, anemia, or tachyarrhythmia, without acute atherothrombosis. Treatment targets the underlying precipitant rather than routine revascularization.

Assay detecting very low troponin concentrations, enabling rapid rule-out protocols. Interpretation requires serial change; a single elevated value indicates injury, not necessarily acute coronary occlusion.

Goal of primary percutaneous coronary intervention within 90 minutes of first medical contact at a PCI-capable center, or fibrinolysis within 30 minutes when timely transfer is impossible. Delay increases myocardial loss.

Combination of renin-angiotensin system inhibition or ARNI, evidence-based beta blocker, mineralocorticoid receptor antagonist, and SGLT2 inhibitor for reduced-ejection-fraction heart failure. Each class improves survival and they are started early.

Low cardiac output from pump failure causing hypoperfusion despite adequate filling, often with elevated filling pressures. In-hospital management may include inotropes, vasopressors, and mechanical circulatory support while treating the cause.

Acute fluctuating disturbance of attention and awareness with agitation or restlessness. Management prioritizes treating the cause, nonpharmacologic measures, and cautious short-term antipsychotics only when safety is threatened.

Set of non-drug interventions including orientation, sleep protection, early mobility, hydration, vision and hearing aids, and family involvement. It reduces incident delirium in hospitalized older adults.

Structured evaluation of consciousness or cognition change using history, medication review, glucose, electrolytes, infection screening, toxicology, and neuroimaging when focal signs or trauma exist. Treat reversible causes first.

Ten-point bedside scale from unarousable to combative that grades sedation and agitation. It guides titration of sedatives and helps distinguish delirium-related agitation from pain or undersedation.

Urgent correction of coagulopathy from anticoagulants to control major bleeding, using agent-specific antidotes such as vitamin K plus four-factor prothrombin complex concentrate for warfarin or andexanet for factor Xa inhibitors.

Temporary use of a short-acting parenteral anticoagulant while a long-acting agent is held before and after surgery. It is reserved for high thrombotic risk because bridging increases bleeding without clear benefit in most patients.

Stroke-risk estimate in atrial fibrillation scoring age, sex, heart failure, hypertension, diabetes, and prior stroke or vascular disease. Higher scores favor anticoagulation.

Bleeding-risk estimate in atrial fibrillation covering hypertension, renal or liver disease, stroke, bleeding history, labile INR, age, and drugs or alcohol. High scores prompt closer monitoring and correction of modifiable factors rather than withholding anticoagulation.

Perioperative tool assigning one point each for ischemic heart disease, heart failure, cerebrovascular disease, diabetes on insulin, renal impairment, and high-risk surgery. Higher totals predict major cardiac complications after noncardiac surgery.

Estimation of exercise tolerance before surgery, often by asking whether a patient can climb two flights of stairs. Poor capacity in patients with cardiac risk factors may warrant further testing.

Acute kidney injury defined by a creatinine rise of at least 0.3 mg/dL within 48 hours, a 1.5-fold rise within seven days, or urine output below 0.5 mL/kg/h for six hours, graded in three stages.

Administration of a weight-based loop diuretic dose to predict progression of acute kidney injury, judged by urine output over the next two hours. Low output suggests intrinsic injury and higher risk of worsening renal function.

Calculated clearance ratio of urea to creatinine used to distinguish prerenal from intrinsic azotemia, especially in patients on diuretics where sodium-based indices mislead. Values below roughly 35 percent suggest prerenal physiology.

Inadequate natriuresis or fluid removal despite escalating loop diuretic doses, often from distal sodium reabsorption, reduced renal perfusion, or gut edema limiting absorption. Strategies include higher doses, continuous infusion, or adding a thiazide.

Restricting sodium rise to roughly 8 to 10 mmol/L in 24 hours to avoid osmotic demyelination, with lower targets in high-risk patients. Overly rapid correction requires relowering or free water administration.

Demyelinating brain injury, classically central pontine, arising from overly rapid correction of chronic hyponatremia. It presents days later with dysarthria, dysphagia, quadriparesis, or locked-in features.

Emergency sequence using intravenous calcium to protect the myocardium, then shifting potassium intracellularly with insulin and glucose or beta agonist, plus removal via diuretics, binders, or dialysis.

Acidosis with elevated calculated anion gap from accumulation of unmeasured acids such as ketones, lactate, uremic toxins, or toxins. The MUDPILES mnemonic frames the differential and guides targeted testing.

Comparison of the rise in anion gap with the fall in bicarbonate, used to detect a coexisting metabolic process. A delta ratio far from 1 to 2 suggests an additional normal-gap or high-gap disorder.

Protocol using isotonic fluids, intravenous insulin after potassium is confirmed adequate, frequent electrolyte replacement, and treatment of precipitants. Bicarbonate is reserved for severe acidemia.

Life-threatening thyrotoxicosis with fever, tachyarrhythmia, agitation, and multiorgan dysfunction. Treatment combines beta blockade, thionamide, iodine given after the thionamide, glucocorticoid, and supportive care.

Acute cortisol deficiency causing hypotension, weakness, and electrolyte derangement, often triggered by infection or surgery. Treatment is prompt parenteral hydrocortisone with fluids and correction of the precipitant.

Use of validated scores and clinical features to identify very low-risk patients suitable for early discharge versus those needing urgent endoscopy and resuscitation. Endoscopy timing and transfusion thresholds follow risk.

Infection of ascitic fluid without a surgical source, diagnosed by polymorphonuclear cell count of 250 or more per microliter. It warrants prompt antibiotics and albumin, plus secondary prophylaxis after recovery.

Vasoconstrictor used with albumin to improve renal perfusion in hepatorenal syndrome by splanchnic vasoconstriction. Patients require monitoring for respiratory failure and ischemia.

Systematic efforts to improve antibiotic selection, dose, route, and duration while limiting unnecessary use. Core activities include prospective audit with feedback, prior authorization, de-escalation, and intravenous-to-oral conversion.

Using serial procalcitonin levels alongside clinical judgment to shorten antibiotic courses in lower respiratory infection and sepsis. It supports stopping decisions but does not by itself mandate starting antibiotics.

Institution-specific summary of susceptibility rates for common pathogens, used to guide empiric therapy before culture results return. Local resistance patterns should be reviewed regularly.

Rapid nasal swab test with high negative predictive value for methicillin-resistant Staphylococcus aureus pneumonia. A negative result supports stopping empiric anti-MRSA therapy in suspected pneumonia.

Prevention package including hand hygiene, full-barrier insertion, chlorhexidine skin antisepsis, optimal site selection, and daily review of line necessity. Adherence reduces bloodstream infections.

Avoiding unnecessary urinary catheters, using aseptic insertion, maintaining closed drainage, and removing devices promptly. Asymptomatic bacteriuria should not be treated except in specific situations.

Risk-stratified use of pharmacologic or mechanical measures to prevent deep vein thrombosis and pulmonary embolism in hospitalized patients. Choice depends on bleeding risk, mobility, and expected length of stay.

Structured transfer of patient information and responsibility between clinicians, using a consistent format covering illness severity, summary, actions, and contingency planning. Poor handoffs contribute to adverse events.

Team-based retrospective method to identify underlying system failures contributing to a serious safety event and to design durable corrective actions. It focuses on processes rather than individual blame.