RAA key terms

The total volume of oxygen reaching the tissues each minute, calculated as cardiac output multiplied by arterial oxygen content. It couples circulation and oxygenation, so falls in output or hemoglobin reduce tissue oxygen supply even when saturation looks normal.

The amount of oxygen carried in each deciliter of arterial blood, mostly bound to hemoglobin plus a small dissolved fraction. It depends on hemoglobin concentration, saturation, and the dissolved oxygen coefficient.

The volume of oxygen the body's tissues extract and use per minute. When delivery falls below consumption, anaerobic metabolism and lactic acidosis develop. Anesthesia generally lowers consumption by reducing metabolic rate and muscle activity.

The volume of gas remaining in the lungs at the end of a normal passive exhalation. It acts as the oxygen reservoir during apnea and is reduced by obesity, pregnancy, supine position, and general anesthesia, hastening desaturation after ventilation stops.

The lung volume at which small airways begin to close during exhalation. When closing capacity exceeds functional residual capacity, airway closure occurs during tidal breathing, producing shunt and hypoxemia, especially in elderly or obese patients and in the supine position.

Blood that passes through the lungs without taking part in gas exchange, as in collapsed alveoli or congenital right-to-left flow. Shunted blood retains venous oxygen content, so supplemental oxygen cannot fully correct the resulting hypoxemia.

The difference between calculated alveolar oxygen partial pressure and measured arterial oxygen partial pressure. It widens with ventilation-perfusion mismatch, shunt, or diffusion impairment and helps distinguish hypoxemia from hypoventilation alone.

A local reflex in which small pulmonary arteries constrict when alveolar oxygen is low, diverting blood toward better-ventilated lung regions. Volatile anesthetics and vasodilators can blunt this reflex, worsening shunt and hypoxemia.

The principle that increasing ventricular filling stretches cardiac muscle and increases the force of contraction, up to a point. It explains why fluid loading raises stroke volume in responders and why overfilling causes congestion without further output gain.

The volume of blood ejected by the heart each minute, equal to heart rate multiplied by stroke volume. Anesthetic drugs, ventilation strategy, blood loss, and depth of anesthesia all influence it, and it is a key determinant of oxygen delivery.

The percentage change in stroke volume across the respiratory cycle during positive-pressure ventilation. Large swings suggest the heart is operating on the steep part of the Frank-Starling curve and may respond to fluid, though arrhythmias and spontaneous effort limit interpretation.

The cyclic change in systolic minus diastolic pressure during mechanical ventilation, used as a dynamic marker of volume responsiveness. Values above roughly 13 percent suggest fluid responsiveness in patients in sinus rhythm with controlled ventilation and adequate tidal volumes.

The average arterial pressure over the cardiac cycle, roughly one-third of pulse pressure added to diastolic pressure. It approximates organ perfusion pressure, and cerebral and renal autoregulation depend on keeping it within an adequate range.

The pressure gradient driving blood flow to the brain, calculated as mean arterial pressure minus intracranial pressure. It falls when intracranial pressure rises or systemic pressure drops, threatening ischemic injury.

The pressure inside the rigid skull exerted by brain tissue, cerebrospinal fluid, and blood. Sustained elevation reduces cerebral perfusion and can cause herniation; carbon dioxide tension and venous drainage strongly affect it.

The alveolar concentration of a volatile anesthetic at which half of patients do not move in response to a standardized surgical stimulus. It allows potency comparison between agents and guides dosing, and it decreases with age, hypothermia, pregnancy, and sedatives.

The phenomenon in which rapid uptake of a high-concentration gas such as nitrous oxide concentrates remaining alveolar gases, accelerating the rise of a concurrently administered volatile agent. It reflects alveolar volume contraction during induction.

The observation that a higher inspired concentration of an anesthetic gas raises its alveolar concentration faster than a proportional increase would predict, because uptake into blood is limited relative to delivery. It shortens induction with potent agents given in high concentrations.

The time required for plasma concentration of a drug given by continuous infusion to fall by half after the infusion stops. It lengthens with infusion duration for drugs that accumulate in peripheral compartments, which matters when choosing infusions for day surgery.

The estimated concentration of a drug at its site of action, such as brain receptors, rather than in plasma. Target-controlled infusion systems model this value because clinical effect lags behind blood concentration after a bolus or rate change.

An anesthetic technique in which hypnosis and often analgesia are maintained entirely by intravenous drugs, typically propofol with an opioid, without inhaled agents. It avoids operating room pollution and suits patients at risk from volatile agents, but requires reliable intravenous access.

A halogenated liquid whose vapor is inhaled to produce unconsciousness and amnesia, such as sevoflurane, isoflurane, or desflurane. These agents also cause dose-dependent vasodilation, respiratory depression, and uterine relaxation.

Administering high inspired oxygen before induction to replace nitrogen in the functional residual capacity with oxygen. It creates a reservoir that prolongs the safe apnea time before desaturation, especially important when difficult mask ventilation or intubation is anticipated.

Continued oxygen uptake through the lungs during apnea when the airway is kept open, driven by mass flow of oxygen into the alveoli as carbon dioxide accumulates. It slows desaturation during intubation attempts but does not remove carbon dioxide.

A structured sequence of plans for managing an airway that cannot be ventilated, intubated, or both, moving from noninvasive to invasive rescue options. It emphasizes limiting attempts, calling for help, and maintaining oxygenation throughout.

The critical situation in which neither tracheal intubation nor mask ventilation succeeds, leaving no route for oxygenation. It is an emergency requiring immediate invasive rescue such as front-of-neck access, because hypoxia and cardiac arrest follow within minutes.

An emergency invasive technique that enters the airway through the anterior neck, by needle or scalpel, to restore oxygenation when upper airway routes fail. It is the final step in a cannot-intubate, cannot-oxygenate sequence.

An induction technique designed to minimize the interval between loss of consciousness and securing the airway, using a fast-acting induction agent and a neuromuscular blocker with cricoid pressure or careful positioning. It is chosen when aspiration risk is high.

Chemical lung injury from inhalation of gastric contents, producing bronchospasm, hypoxemia, and a chemical burn to the airways. Risk rises with full stomach, delayed gastric emptying, obesity, pregnancy, and inadequate airway protection during induction or emergence.

Pressure applied to the cricoid cartilage to compress the esophagus and reduce passive regurgitation during induction. Its effectiveness is debated, it can worsen laryngoscopy views, and it is released if it impedes ventilation or intubation.

Paralysis produced by drugs that interrupt transmission at the motor end plate, either depolarizing or nondepolarizing. It facilitates intubation and surgery but requires monitoring of depth and reversal, because residual block risks aspiration and respiratory failure.

Peripheral nerve stimulation delivering four supramaximal twitches to assess the depth of neuromuscular blockade. The ratio of the fourth to the first response estimates recovery, and a ratio above 0.9 is generally needed before safe extubation.

A modified cyclodextrin that encapsulates and inactivates aminosteroid muscle relaxants such as rocuronium and vecuronium, reversing even deep blockade within minutes. It cannot reverse depolarizing agents and carries a risk of anaphylaxis and bradycardia.

A genetic disorder in which volatile anesthetics or succinylcholine trigger uncontrolled skeletal muscle calcium release, causing hyperthermia, rigidity, acidosis, and hyperkalemia. Treatment is dantrolene plus supportive measures and removal of the triggering agent.

A muscle relaxant that blocks calcium release from the sarcoplasmic reticulum and is the specific antidote for malignant hyperthermia. It is given intravenously in repeated doses until hyperthermia and rigidity resolve, alongside cooling and supportive care.

A dose-related syndrome from excess local anesthetic in blood, beginning with perioral numbness, tinnitus, and agitation and progressing to seizures, coma, arrhythmias, and cardiac arrest. Treatment includes airway support and intravenous lipid emulsion.

A rescue therapy for local anesthetic systemic toxicity, given as a bolus and infusion of lipid to sequester the drug and support cardiac function. It is used together with standard resuscitation and airway management.

A metabolic acidosis caused by excess lactate, produced when tissue oxygen demand exceeds supply or when lactate clearance is impaired. In the perioperative setting it signals poor perfusion, hypoxia, or other serious pathology.

An abnormally low partial pressure of oxygen in arterial blood, detected by blood gas analysis or inferred from pulse oximetry. Causes include hypoventilation, ventilation-perfusion mismatch, shunt, and diffusion impairment, and it may occur without visible cyanosis.

Ventilation in excess of metabolic need, lowering arterial carbon dioxide and raising pH. In neuroanesthesia it is used briefly to reduce intracranial pressure by cerebral vasoconstriction, but prolonged use risks cerebral ischemia.

A noninvasive method that estimates arterial hemoglobin oxygen saturation by comparing light absorption at two wavelengths across a pulsatile vascular bed. It is affected by poor perfusion, motion, dyshemoglobins, and nail polish, and it does not measure ventilation.

Continuous measurement and display of carbon dioxide in respired gas, usually as a waveform. It confirms tracheal tube placement, detects disconnection and obstruction, and reflects cardiac output and metabolism as well as ventilation.

The partial pressure of carbon dioxide measured at the end of exhalation, normally close to arterial carbon dioxide in healthy lungs. A sudden fall suggests disconnection, hypotension, or embolism, while a rise suggests hypoventilation or increased metabolism.

Collapse or incomplete expansion of lung tissue, common after general anesthesia and in the supine position. It creates shunt and lowers functional residual capacity, contributing to postoperative hypoxemia and infection.

Nausea or vomiting occurring after anesthesia and surgery, driven by anesthetic agents, opioids, pain, hypotension, and patient factors such as female sex and nonsmoking status. Prevention uses risk scores and multimodal antiemetics.

The recovery area where patients are monitored after anesthesia until vital signs, consciousness, and airway reflexes are stable. Care includes oxygen, pain and nausea control, temperature management, and early detection of complications such as bleeding or airway obstruction.

A standardized assessment of readiness for discharge from recovery, scoring activity, breathing, circulation, consciousness, and oxygen saturation. Higher totals indicate fitness for transfer to a ward or home.

Combining analgesics with different mechanisms, such as local anesthetics, nonsteroidal agents, acetaminophen, and opioids, to improve pain relief while reducing opioid dose and side effects. It is a core principle of enhanced recovery protocols.

The strategy of using nonopioid drugs and regional techniques to reduce or eliminate opioid requirements. It lowers opioid-related respiratory depression, sedation, nausea, and ileus while still achieving adequate pain control.