EDAIC Part I key terms

The volume of gas remaining in the lungs at the end of a normal passive expiration. It results from the balance between outward chest wall recoil and inward lung elastic recoil, and is the reservoir for gas exchange during apnoea.

The lung volume at which small airways begin to close during expiration. When it exceeds functional residual capacity, airway closure occurs during tidal breathing, causing shunt and hypoxaemia, particularly in elderly or obese patients and in the supine position.

The change in volume produced by a given change in distending pressure, expressed in millilitres per centimetre of water. Static compliance reflects lung and chest wall elasticity, while dynamic compliance also includes airway resistance during inflation.

The pressure gradient required to drive a given gas flow through the airways, usually expressed in centimetres of water per litre per second. It rises with bronchoconstriction, secretions, and low lung volumes, and is largely determined by large airways.

The proportion of cardiac output that passes through the lungs without taking part in gas exchange, mixing deoxygenated blood with arterial blood. It is calculated from the shunt equation and is poorly responsive to supplemental oxygen when large.

The difference between calculated alveolar oxygen partial pressure and measured arterial oxygen partial pressure. It widens with ventilation-perfusion mismatch, shunt, and diffusion impairment, and helps distinguish hypoxaemia due to hypoventilation from intrinsic lung disease.

A relationship estimating alveolar oxygen partial pressure from inspired oxygen pressure, arterial carbon dioxide pressure, and the respiratory quotient. It underpins calculation of the alveolar-arterial gradient and assessment of oxygenation efficiency.

The total amount of oxygen transported to the tissues each minute, the product of cardiac output and arterial oxygen content. Content depends mainly on haemoglobin concentration and saturation, so anaemia and low output both reduce delivery.

The volume of oxygen taken up by the body per minute, normally about 250 millilitres at rest and rising several-fold with sepsis, shivering, or exercise. When consumption exceeds delivery, anaerobic metabolism and lactic acidosis develop.

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, though it can be misleading in regional ischaemia or shunting.

Oxygen saturation sampled from the superior vena cava or right atrium, used as a surrogate for mixed venous saturation. It is usually slightly higher than true mixed venous blood because it drains the brain and kidneys, which extract less oxygen.

The administration of high inspired oxygen before induction of anaesthesia to replace nitrogen in the functional residual capacity with oxygen. This creates a larger safe apnoea time before desaturation occurs during airway management.

Collapse or loss of aeration of lung tissue, commonly occurring in dependent regions during general anaesthesia and after cardiac or abdominal surgery. It contributes to shunt, reduced compliance, and postoperative pulmonary complications.

A positive pressure maintained in the airways at end-expiration during mechanical ventilation. It recruits collapsed alveoli, increases functional residual capacity, and improves oxygenation, but can reduce venous return and cause barotrauma.

The unintentional retention of positive pressure in the alveoli at end-expiration, also called intrinsic PEEP. It arises when expiratory time is insufficient, as in asthma or high minute ventilation, and can cause hypotension and increased work of breathing.

Progressive increase in lung volume over successive breaths when expiration is incomplete before the next breath begins. It raises intrathoracic pressure, impairs venous return, and can precipitate hypotension or cardiac arrest in severe obstructive disease.

A ventilator mode delivering a set tidal volume at a set rate, with airway pressure determined by compliance and resistance. It guarantees minute ventilation but may generate high pressures if the lungs are stiff.

A ventilator mode delivering gas at a set inspiratory pressure for a set time, with tidal volume dependent on compliance and resistance. It produces decelerating flow and may improve distribution but requires monitoring of delivered volume.

The proximal airway pressure measured during an end-inspiratory pause, reflecting alveolar pressure when flow has ceased. It is used to estimate the risk of ventilator-induced lung injury, with values above about thirty centimetres of water considered potentially harmful.

The difference between plateau pressure and applied positive end-expiratory pressure. It reflects the cyclic stretch applied to the lung per breath and is associated with mortality in acute respiratory distress syndrome, independent of tidal volume.

An acute inflammatory lung injury causing bilateral opacities, severe hypoxaemia, and reduced compliance that cannot be fully explained by cardiac failure. Management emphasises lung-protective ventilation, prone positioning in severe cases, and treatment of the underlying cause.

A transient increase in airway pressure designed to reopen collapsed alveoli, often followed by adequate positive end-expiratory pressure to keep them open. It may improve oxygenation but carries risks of hypotension and barotrauma.

A technique for inducing anaesthesia in patients at risk of aspiration, using a rapidly acting induction agent followed promptly by tracheal intubation with minimal interval for positive-pressure ventilation. Cricoid pressure and preoxygenation are often included.

A depolarising neuromuscular blocking agent with the fastest onset and shortest duration of the commonly used relaxants. It is used for rapid sequence induction but can cause hyperkalaemia, bradycardia, and malignant hyperthermia, and is contraindicated in burns and denervation.

Pharmacological paralysis produced by drugs that interfere with transmission at the motor end plate, either depolarising or non-depolarising. Depth is monitored with peripheral nerve stimulation, and residual block must be excluded before extubation.

The ratio of the fourth to the first evoked muscle response during four supramaximal stimuli delivered to a peripheral nerve. A ratio above 0.9 indicates adequate recovery from neuromuscular blockade before extubation.

An acetylcholinesterase inhibitor used to reverse non-depolarising neuromuscular blockade by increasing acetylcholine at the motor end plate. It is given with an antimuscarinic to prevent bradycardia and is ineffective against deep block.

A modified gamma-cyclodextrin that encapsulates rocuronium and vecuronium, rapidly reversing even deep neuromuscular blockade. It avoids the ceiling effect of acetylcholinesterase inhibitors but can cause anaphylaxis and bradycardia.

A pharmacogenetic hypermetabolic crisis triggered by volatile anaesthetics and depolarising relaxants, caused by uncontrolled calcium release in skeletal muscle. Features include rising temperature, rigidity, hypercapnia, and acidosis, treated with dantrolene and supportive care.

The specific treatment for malignant hyperthermia, acting by inhibiting calcium release from the sarcoplasmic reticulum of skeletal muscle. It is given intravenously in repeated doses until the crisis is controlled, alongside cooling and correction of acidosis.

Chemical injury to the lungs caused by inhalation of gastric contents, producing bronchospasm, hypoxaemia, and pulmonary oedema within hours. Management is supportive, with airway protection, oxygen, and ventilation as required; antibiotics are reserved for infection.

Reflex closure of the vocal cords caused by stimulation of the laryngeal nerves, often during light anaesthesia, airway manipulation, or extubation. It is managed with continuous positive airway pressure, deepening anaesthesia, or small doses of a muscle relaxant.

The volume of blood ejected by the heart each minute, the product of heart rate and stroke volume. It determines oxygen delivery and is influenced by preload, contractility, and afterload.

The percentage change in stroke volume over the respiratory cycle during positive-pressure ventilation. A large variation suggests fluid responsiveness in patients in sinus rhythm with controlled ventilation, but it is unreliable in spontaneous breathing or arrhythmia.

The observation that increasing ventricular filling (preload) increases stroke volume up to a point, after which further filling gives little additional output. It guides fluid therapy and explains why fluid responsiveness depends on where the ventricle sits on this curve.

An end product of anaerobic glucose metabolism that rises when tissue oxygen delivery is inadequate or when metabolism is altered, as in sepsis. Clearance over time is used as a marker of resuscitation response and prognosis.

Life-threatening organ dysfunction caused by a dysregulated host response to infection. Management includes prompt antimicrobials, source control, fluid resuscitation, and vasopressors, with attention to oxygen delivery and lactate clearance.

Sepsis with persisting hypotension requiring vasopressors to maintain mean arterial pressure and a raised lactate despite adequate fluid resuscitation. It carries high mortality and reflects profound circulatory and metabolic derangement.

A predominantly alpha-adrenergic vasopressor used first line in septic and other vasodilatory shock to restore mean arterial pressure. It increases systemic vascular resistance with modest effects on cardiac output and is titrated to a pressure target.