Iran Anesthesiology Specialty Board Exam key terms

The volume of gas remaining in the lungs at the end of a normal passive expiration. It is the sum of expiratory reserve volume and residual volume, and it determines the oxygen reservoir available during apnea.

The lung volume at which small airways begin to close during expiration. When it exceeds functional residual capacity, as in supine patients, obesity, or infants, airway closure occurs during tidal breathing and promotes atelectasis and shunt.

The fraction of cardiac output that passes through unventilated lung units and therefore returns to the left heart without taking up oxygen. It causes hypoxemia that responds poorly to increasing inspired oxygen.

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

The alveolar concentration of an inhaled anesthetic at which 50 percent of patients do not move in response to a standard surgical stimulus. It allows comparison of potency among volatile agents and is reduced by age, hypothermia, and sedatives.

The time required for plasma concentration of an infused drug to fall by half after stopping the infusion. It lengthens as infusion duration increases for drugs with slow redistribution, guiding recovery prediction for propofol and remifentanil.

The estimated drug concentration at the site of action, typically the brain, used in target-controlled infusion. It lags behind plasma concentration because of circulation and drug transfer delay, so it better predicts clinical effect.

The phenomenon in which rapid uptake of a high-concentration gas such as nitrous oxide accelerates the rise in alveolar concentration of a concurrently administered volatile agent. It results from concentration and volume effects in the alveolus.

The resistance opposing blood flow through the pulmonary circulation. It is increased by hypoxemia, hypercarbia, acidosis, and high airway pressure, which is important when ventilating patients with right ventricular dysfunction or pulmonary hypertension.

Right ventricular enlargement and dysfunction caused by pulmonary hypertension from lung disease. In anesthesia it predicts poor tolerance of hypoxemia, hypercarbia, and positive-pressure ventilation, and it raises the risk of cardiovascular collapse during induction.

The principle that increasing ventricular end-diastolic volume, within physiologic limits, increases stroke volume. It underlies fluid responsiveness assessment and explains why excessive filling eventually reduces output in failing ventricles.

The cyclic percentage change in stroke volume during mechanical ventilation, reflecting heart-lung interaction. High variation in a fully ventilated patient with regular rhythm suggests fluid responsiveness, provided filling pressures and tidal volumes are adequate.

The synapse between a motor nerve terminal and skeletal muscle fiber where acetylcholine released into the synaptic cleft binds nicotinic receptors to trigger contraction. It is the site of action of depolarizing and nondepolarizing muscle relaxants.

The ratio of the fourth to the first evoked muscle response to four supramaximal stimuli delivered at 2 Hz. A ratio above 0.9 indicates adequate recovery from neuromuscular blockade and reduces postoperative residual weakness.

A modified gamma-cyclodextrin that encapsulates rocuronium and vecuronium in plasma, rapidly reversing even deep neuromuscular blockade. It is ineffective against benzylisoquinolinium relaxants such as cisatracurium and can cause anaphylaxis and bradycardia.

The product of cardiac output and arterial oxygen content, representing oxygen transported to tissues per minute. It depends mainly on hemoglobin concentration, saturation, and cardiac output, and falls when any of these is reduced.

The oxygen saturation of blood in the pulmonary artery, reflecting the balance between whole-body oxygen delivery and consumption. A low value suggests inadequate delivery or increased demand, while a high value may indicate sepsis-related extraction failure.

Deliberate acceptance of elevated arterial carbon dioxide during mechanical ventilation, achieved with low tidal volumes, to limit lung injury or reduce intrathoracic pressure. It is avoided in raised intracranial pressure and severe pulmonary hypertension.

A ventilation strategy using low tidal volumes based on predicted body weight, limited plateau pressure and driving pressure, and appropriate positive end-expiratory pressure. It reduces ventilator-induced lung injury in acute respiratory distress syndrome and in intraoperative one-lung ventilation.

Ventilation of a single lung, usually achieved with a double-lumen tube or bronchial blocker, to isolate and rest the operative lung. It requires lung-protective settings and vigilance for hypoxemia from shunt through the nonventilated lung.

A device passed through or alongside a single-lumen tracheal tube to occlude a main bronchus and achieve lung isolation. It is useful when a double-lumen tube is unsuitable, but deflation and positioning require bronchoscopic confirmation.

A technique for urgent airway control in patients at risk of aspiration, using preoxygenation, a rapid-onset induction agent, and a fast-acting neuromuscular blocker with minimal mask ventilation before intubation. Cricoid pressure is often applied but its benefit is debated.

Chemical lung injury from inhalation of gastric contents, typically acidic and particulate, causing bronchospasm, hypoxemia, and infiltrates within hours. Management is supportive, and routine prophylactic antibiotics or steroids are not recommended.

A structured sequence of planned options for unanticipated difficulty with ventilation, supraglottic rescue, intubation, or emergency front-of-neck access. It emphasizes limiting attempts, calling for help, and maintaining oxygenation throughout.

A life-threatening emergency in which tracheal intubation and all noninvasive oxygenation methods have failed. Immediate emergency front-of-neck access, such as scalpel-bougie-tube cricothyrotomy, is required to prevent hypoxic brain injury and death.

A positional headache worsened by upright posture and relieved by lying flat, caused by cerebrospinal fluid leakage after dural puncture. It is managed initially with hydration, caffeine, and analgesics, and definitively with an epidural blood patch.

Injection of autologous blood into the epidural space near the site of dural puncture to seal the leak. It relieves postdural puncture headache in most patients and is most effective when performed at least 24 hours after the puncture.

A dose-related syndrome of neurologic excitation followed by depression and cardiovascular collapse after local anesthetic absorption or intravascular injection. Treatment includes airway support, benzodiazepines, lipid emulsion rescue, and avoidance of vasopressin and calcium channel blockers.

Intravenous administration of a lipid emulsion as an antidote for local anesthetic systemic toxicity, given as a bolus followed by infusion. It is thought to create a lipid sink and support myocardial energetics, and should be given early in severe toxicity.

A pharmacogenetic hypermetabolic crisis triggered by volatile anesthetics and succinylcholine, caused by abnormal skeletal muscle calcium release. Features include hypercarbia, rigidity, hyperthermia, and acidosis; treatment is dantrolene plus aggressive supportive care.

A skeletal muscle relaxant that inhibits calcium release from the sarcoplasmic reticulum and is the specific antidote for malignant hyperthermia. It is given intravenously in repeated doses until hypercarbia, rigidity, and temperature are controlled.

A multimodal perioperative pathway combining preoperative counseling, opioid-sparing analgesia, early feeding, and early mobilization to reduce complications and shorten hospital stay. It relies on audit of process and outcome measures for continuous improvement.

The combined use of analgesic drugs and techniques with different mechanisms, such as regional blocks, acetaminophen, nonsteroidal agents, and opioids, to improve pain relief while reducing opioid dose and adverse effects.

An acute focal neurologic deficit of vascular origin occurring during or within 30 days after surgery. Risk is increased by carotid disease, atrial fibrillation, prior stroke, and hypotension, and it requires urgent imaging and multidisciplinary management.

Myocardial injury with ischemia occurring during or after surgery, often silent and detected by troponin and electrocardiography. It is associated with major bleeding, hypotension, and anemia, and carries high short-term mortality.

A severe IgE-mediated or non-IgE-mediated hypersensitivity reaction during anesthesia, commonly triggered by neuromuscular blockers, antibiotics, chlorhexidine, or latex. Hypotension and bronchospasm dominate; treatment is epinephrine, fluids, and withdrawal of the trigger.