CRT (IJCAHPO) key terms

The volume of gas inhaled or exhaled during one normal, resting breath. It is the basic building block of minute ventilation and is typically set on a ventilator to match the patient's metabolic needs.

The total volume of gas moved into and out of the lungs per minute, calculated as tidal volume multiplied by respiratory rate. It reflects overall breathing effort and CO2 clearance capability.

The portion of minute ventilation that reaches gas-exchanging alveoli rather than dead space. It is calculated as respiratory rate times the difference between tidal volume and dead space volume, and it determines CO2 elimination.

The fraction of each breath that fills conducting airways or unperfused alveoli and never participates in gas exchange. Increased dead space raises the ventilation needed to maintain normal carbon dioxide levels.

The sum of anatomic dead space (conducting airways) and alveolar dead space (ventilated but unperfused alveoli). It is estimated clinically using the Bohr equation from measured CO2 values.

A measure of how readily the lungs or chest wall distend in response to a change in pressure, expressed as volume change per unit pressure change. Low compliance means stiffer lungs requiring more pressure to inflate.

The opposition to gas flow through the airways, determined by pressure difference divided by flow. Increased resistance from bronchospasm, secretions, or a narrow artificial airway raises the pressure needed to deliver a given flow.

The tendency of the lungs and chest wall to recoil to their resting volume; it is the reciprocal of compliance. Higher elastance means the tissue resists stretching and generates more recoil pressure at a given volume.

The inward cohesive force at the liquid lining of the alveoli that promotes alveolar collapse. Pulmonary surfactant reduces this force, stabilizing alveoli and lowering the pressure required to keep them open.

A phospholipid substance produced by type II alveolar cells that lowers surface tension, preventing alveolar collapse and reducing the work of breathing. Deficiency causes atelectasis and stiff lungs.

The principle that at a constant temperature, the pressure of a gas is inversely proportional to its volume. It explains how diaphragm descent and chest expansion lower intrathoracic pressure and draw gas into the lungs.

The principle that the total pressure of a gas mixture equals the sum of the partial pressures of its component gases. It is used to calculate the partial pressure of oxygen in a delivered gas mixture.

The principle that the amount of gas dissolved in a liquid is proportional to the partial pressure of that gas above the liquid and to its solubility. It explains how alveolar oxygen and nitrogen enter and leave blood.

The pressure exerted by one gas within a mixture, which drives its movement between compartments such as alveoli and blood. Oxygen moves down its partial pressure gradient from alveolus into capillary blood.

The passive movement of gas molecules from an area of higher partial pressure to one of lower partial pressure across the alveolar-capillary membrane. It is impaired by thickened membranes, low surface area, or reduced driving pressure.

The relationship between the amount of air reaching the alveoli and the amount of blood flowing through their capillaries. Mismatch, either shunt or dead space, is the most common cause of hypoxemia.

Blood that passes through the pulmonary circulation without participating in gas exchange, as in atelectasis or an intracardiac defect. Shunt causes hypoxemia that responds poorly to supplemental oxygen.

An abnormally low partial pressure of oxygen in arterial blood, conventionally a PaO2 below about 80 mmHg on room air. It is caused by hypoventilation, V/Q mismatch, shunt, diffusion impairment, or low inspired oxygen.

Hypoxemia that persists despite increasing the fraction of inspired oxygen. It suggests a true shunt, because blood bypassing ventilated alveoli cannot be oxygenated by raising inspired oxygen alone.

A condition in which hemoglobin iron is oxidized to the ferric state and cannot carry oxygen, causing cyanosis and falsely normal pulse oximetry readings. It may be treated with methylene blue.

Hemoglobin bound to carbon monoxide, which has a much higher affinity than oxygen and reduces oxygen-carrying capacity. Pulse oximetry cannot distinguish it from oxyhemoglobin, so readings appear falsely normal.

A graph relating oxygen saturation to partial pressure of oxygen in blood, with its sigmoid shape reflecting cooperative binding. Shifts affect how readily oxygen is loaded in the lungs and unloaded at tissues.

The partial pressure of oxygen at which hemoglobin is 50 percent saturated, normally about 27 mmHg. A higher P50 indicates reduced affinity and easier oxygen unloading; a lower P50 indicates increased affinity.

The shift of the oxyhemoglobin dissociation curve caused by changes in carbon dioxide and hydrogen ion concentration. Increased CO2 and acidity reduce hemoglobin's oxygen affinity, enhancing oxygen release to active tissues.

The phenomenon in which deoxygenated hemoglobin carries more carbon dioxide than oxygenated hemoglobin. It aids carbon dioxide pickup in tissues and release in the lungs.

The combined distensibility of lungs and chest wall, measured as volume change divided by the change in transthoracic pressure. It is assessed at the bedside by dividing tidal volume by plateau pressure minus positive end-expiratory pressure.

The highest airway pressure reached during a delivered breath, reflecting both airway resistance and lung compliance. Rising PIP with a stable plateau suggests increased airway resistance such as secretions or bronchospasm.

The airway pressure measured during a brief inspiratory pause when flow has ceased, reflecting alveolar distending pressure. It guides safe ventilator settings and estimates the risk of ventilator-induced lung injury.

A positive pressure maintained in the airways at the end of exhalation that keeps alveoli open and improves oxygenation. It increases functional residual capacity but can reduce venous return and cardiac output.

Positive pressure trapped in the alveoli at end-exhalation because the next breath begins before the previous one fully empties. It is common in obstructive disease and with high respiratory rates or short expiratory times.

Retention of gas in the lungs because exhalation is incomplete before the next inspiration begins. It raises intrathoracic pressure, can cause dynamic hyperinflation, and may impair venous return and blood pressure.

Progressive increase in end-expiratory lung volume during rapid breathing when exhalation cannot keep pace with inspiration. It increases the work of breathing and can cause hypotension in ventilated patients.

The volume of gas remaining in the lungs at the end of a normal passive exhalation, representing the balance point between lung recoil and chest wall expansion. It is the reservoir for gas exchange between breaths.

The lung volume at which small airways begin to close during exhalation. When closing volume exceeds functional residual capacity, airway closure causes atelectasis and impaired oxygenation.

A brief controlled increase in airway pressure intended to reopen collapsed alveoli and improve oxygenation. It is used cautiously because it can cause barotrauma or hemodynamic compromise.

Lung injury caused by excessive pressure or overdistention during mechanical ventilation, which can produce pneumothorax, pneumomediastinum, or subcutaneous emphysema. Limiting plateau pressure reduces the risk.

Alveolar injury produced by overdistention from excessive tidal volume rather than pressure alone. It is prevented by using lung-protective tidal volumes based on predicted body weight.

Lung injury caused by repeated opening and closing of unstable alveoli during ventilation. Adequate positive end-expiratory pressure helps keep alveoli recruited and reduces this shear stress.

The pressure difference between the airway opening and the alveoli divided by the gas flow rate. It is estimated at the bedside from the difference between peak and plateau pressure during constant-flow ventilation.

A low-density gas mixture of helium and oxygen that reduces turbulent flow and airway resistance. It can lower the work of breathing in upper airway obstruction or severe bronchospasm.

Administration of medication as suspended particles inhaled into the airways, influenced by particle size, device, and breathing pattern. Optimal particles are roughly one to five micrometers and deposit in the lower airways.

The particle size at which half the aerosol mass is contained in larger particles and half in smaller ones. It predicts where particles deposit within the respiratory tract and the efficiency of drug delivery.

A noninvasive method that estimates arterial oxygen saturation by measuring light absorption of oxygenated and deoxygenated hemoglobin across a pulsatile vascular bed. It is affected by poor perfusion, motion, and abnormal hemoglobins.

Continuous measurement and display of the carbon dioxide concentration in exhaled gas, producing a waveform over time. It confirms airway placement, assesses ventilation, and can suggest low cardiac output or obstruction.

The partial pressure of carbon dioxide measured at the end of exhalation, approximating alveolar and arterial CO2 in healthy lungs. A sudden drop may indicate airway disconnection, esophageal intubation, or cardiac arrest.

The proportion of oxygen in the gas a patient inhales, expressed as a decimal or percentage. It is adjusted to maintain adequate arterial oxygenation while minimizing oxygen toxicity.