ABA Critical Care key terms

Acute respiratory failure within one week of a known insult, with bilateral opacities not fully explained by heart failure, and hypoxemia graded by the ratio of arterial oxygen to inspired oxygen on at least 5 cm H2O PEEP.

Plateau pressure minus positive end-expiratory pressure. It estimates the cyclic stress applied to aerated lung during each breath and predicts mortality in ARDS; values above about 15 cm H2O are usually avoided.

Airway pressure held above atmospheric at end-expiration during mechanical ventilation. It keeps alveoli open, improves oxygenation, and reduces repeated collapse, but high levels raise intrathoracic pressure, lower venous return, and can cause barotrauma.

Placing a ventilated patient face down, typically for 12 to 16 hours per session. In moderate-to-severe ARDS it improves survival by making lung inflation more uniform and reducing compression of dorsal lung by the heart and abdomen.

A period of minimal ventilator support, usually 30 to 120 minutes of low pressure support or a T-piece, used to decide whether a patient can breathe unaided before extubation.

Pressure measured in the superior vena cava or right atrium, often used as a rough estimate of right heart filling. It poorly predicts fluid responsiveness because it also depends on venous tone, intrathoracic pressure, and ventricular compliance.

The change in pulse pressure across a respiratory cycle, expressed as a percentage. Large variation in a paralyzed, fully ventilated patient with sinus rhythm suggests fluid responsiveness; arrhythmias, spontaneous breaths, and small tidal volumes make it unreliable.

Compression of the heart by pericardial fluid under pressure, impairing diastolic filling and lowering cardiac output. Findings include hypotension, raised jugular venous pressure, muffled heart sounds, pulsus paradoxus, and echocardiographic chamber collapse.

Pressure inside the rigid adult skull, normally below about 15 mm Hg. Because the skull has fixed volume, added blood, brain swelling, or mass raises pressure, reducing cerebral perfusion and risking herniation.

Mean arterial pressure minus intracranial pressure. It is the pressure gradient driving cerebral blood flow and is commonly targeted at 60 to 70 mm Hg after traumatic brain injury, balancing hypotension against excessive vasopressor use.

Deliberate control of core temperature, usually between 32 and 36 degrees Celsius, for hours to days after cardiac arrest or in selected brain injury. Shivering, bradycardia, electrolyte shifts, and infection are common complications.

Continuous seizure activity lasting five minutes or longer, or repeated seizures without recovery of consciousness between them. It is an emergency treated with benzodiazepines, then antiseizure drugs, while airway, glucose, and triggers are addressed.

An acute, fluctuating disturbance of attention and awareness occurring during critical illness. It predicts longer ventilation, higher mortality, and later cognitive decline; treatment targets causes such as pain, sedation, infection, and sleep disruption.

Irreversible loss of all cerebral and brainstem function, including the drive to breathe, in a patient with a known cause and no confounders such as sedatives, hypothermia, or severe metabolic derangement. Diagnosis uses clinical testing and an apnea test.

An abrupt fall in kidney function, defined by a rising serum creatinine or falling urine output over hours to days. Causes are prerenal, intrinsic renal, or postrenal; care focuses on restoring perfusion and stopping nephrotoxins.

Slow, continuous extracorporeal removal of solute and fluid, usually chosen for hemodynamically unstable patients who tolerate intermittent dialysis poorly. It gives gentle fluid removal and stable osmolality but needs continuous anticoagulation and close monitoring.

Metabolic acidosis with a widened difference between measured cations and anions, reflecting accumulation of acids such as lactate, ketones, or toxins. The gap narrows the differential and should be adjusted for low albumin.

Serum potassium above roughly 5.5 mmol/L, which slows cardiac conduction and can cause fatal arrhythmia. Emergency care combines calcium to stabilize membranes, insulin with glucose or beta agonists to shift potassium into cells, and removal.

Serum sodium below 135 mmol/L, usually caused by excess water rather than sodium loss. Symptoms guide urgency; correcting chronic hyponatremia too quickly can cause osmotic demyelination, so rates are kept slow.

Life-threatening organ dysfunction caused by a dysregulated host response to infection, identified clinically by an acute rise of two or more points in the Sequential Organ Failure Assessment score. Treatment is early antibiotics, source control, and hemodynamic support.

Sepsis with persisting hypotension that needs vasopressors to keep mean arterial pressure at least 65 mm Hg, together with lactate above 2 mmol/L despite adequate fluid resuscitation. Mortality is high and resuscitation must be prompt.

The fall in blood lactate during resuscitation, usually expressed as a percentage of the initial value. Falling lactate suggests improving tissue perfusion; persistent elevation points to ongoing shock, inadequate source control, or impaired liver clearance.

Pneumonia developing more than 48 hours after endotracheal intubation, usually from microaspiration of colonized oropharyngeal secretions. Prevention includes head-of-bed elevation, oral care, light sedation, and avoiding unnecessary ventilator circuit changes.

Fever in a patient whose absolute neutrophil count is below about 500 cells per microliter. It is an emergency: cultures are drawn and broad-spectrum antibiotics started promptly, because bacterial infection can progress within hours.

Widespread activation of coagulation that consumes platelets and clotting factors, producing thrombosis and bleeding together. It accompanies sepsis, major trauma, malignancy, and obstetric emergencies; treatment centers on the underlying cause with support for bleeding.

An immune, antibody-mediated fall in platelets occurring typically five to ten days after heparin exposure, which paradoxically causes thrombosis rather than bleeding. Heparin is stopped immediately and a non-heparin anticoagulant started while testing proceeds.

A preplanned, standardized approach to replacing blood products rapidly in severe hemorrhage, using balanced ratios of red cells, plasma, and platelets plus tranexamic acid and calcium, with frequent laboratory monitoring to limit dilutional coagulopathy and hypothermia.

Acute insulin deficiency producing hyperglycemia, ketone accumulation, and an anion gap metabolic acidosis, often triggered by infection or stopping insulin. Treatment is intravenous fluid, insulin infusion, and aggressive potassium replacement, with dextrose added as glucose falls.

Acute cortisol deficiency causing hypotension, weakness, nausea, hyponatremia, and hyperkalemia, often unmasked by infection, surgery, or steroid withdrawal. Treatment is immediate intravenous hydrocortisone after a cortisol sample, plus fluid and glucose.

Sustained intra-abdominal pressure above 20 mm Hg with new organ dysfunction, often after massive resuscitation, pancreatitis, or trauma. It impairs ventilation, venous return, and kidney perfusion; decompressive laparotomy is definitive when medical measures fail.

A strategy for major hemorrhage that pairs rapid hemorrhage control with permissive hypotension, minimal crystalloid, early balanced blood products, and correction of hypothermia, acidosis, and coagulopathy before definitive surgical repair.

Breakdown of skeletal muscle that releases myoglobin and cell contents into blood, causing dark urine, high creatine kinase, hyperkalemia, hyperphosphatemia, and acute kidney injury. Treatment is early aggressive intravenous fluid and correction of electrolytes.

Dangerous shifts of phosphate, potassium, magnesium, and fluid after nutrition is restarted in a malnourished patient. Risk is reduced by correcting electrolytes first, giving thiamine, and increasing calories slowly with close monitoring.

Rapid loss of hepatic synthetic and detoxifying function in a patient without cirrhosis, producing coagulopathy, encephalopathy, and jaundice. Care includes treating cerebral edema, hypoglycemia, and infection, avoiding sedatives, and early transplant referral.

A recognizable pattern of vital signs, mental status, pupils, skin, and bowel sounds that points to a class of poisoning such as opioid, anticholinergic, sympathomimetic, or cholinergic, guiding treatment before laboratory confirmation.

New or worsening physical, cognitive, or psychological impairment that persists after critical illness and its treatment. It affects survivors and their families; prevention relies on early mobility, lighter sedation, delirium prevention, and structured follow-up.

A person legally authorized to make health care choices for a patient who lacks capacity, ideally following the patient's expressed wishes and values. When these are unknown, decisions rest on best interests and may need ethics consultation.

A primary bloodstream infection in a patient with a central venous catheter that is not explained by another site. Prevention bundles combine hand hygiene, full-barrier insertion, chlorhexidine skin preparation, and daily review of whether the line is still needed.