MECHANICS/PHYSIOLOGY OF BREATHING

1. Respiratory drive: The normal respiratory rate is 12-20 bpm. Respiratory drive is controlled by central and peripheral receptors based on arterial concentrations of carbon dioxide (CO2); oxygen (O2), and hydrogen ions. Increased intracranial pressure, administration of opioids and other medications may cause a central decrease in respiratory drive. This could result in insufficient ventilation to maintain an adequate level of oxygenation and clearance of CO2.1-3
2. Work of breathing: Work of breathing is the mechanical work needed to maintain oxygenation and ventilation. Pain, acidosis, and hypermetabolic states will cause an increased work of breathing. This is not necessarily pathologic but does indicate additional respiratory support is needed while working up the underlying etiology. Prolonged tachypnea, with etiology undiagnosed and untreated, can lead to inspiratory muscle fatigue which could require mechanical ventilator support (e.g., hemorrhagic shock, severe rib fractures, untreated asthma, etc.) 1-3
3. Lung compliance: Lung compliance is the ability of the lung to expand when given a certain amount of air pressure. The more compliant the lung, the less pressure needed for it to expand to a certain volume. Lungs with low compliance will require higher pressures to expand to the same volume as a normal lung. Internal causes such as pneumothorax and fluid/blood in the alveoli can decrease lung compliance. There are also external causes that decrease lung’s ability to expand due to the stiffness of the chest wall, such as obesity, pregnancy, burns, chest wall injury.1-5 A decrease in lung compliance from any cause can lead to hypoxemia and hypercapnia.
4. Tidal volume (TV or VT): Is the volume of air that is exchanged in one breath. Decreases in tidal volume can result from external pressure (i.e. Pneumothorax, hemothorax, tension pneumothorax) by effectively reducing lung volume. Dynamic hyperinflation also known as “breath stacking” is caused by the inability to completely exhale and can lead to “auto-positive end expiratory pressure (auto-PEEP).” This may be due to inadequate exhalation time, airflow obstruction, or both. This condition leads to decreasing tidal volumes and can cause hemodynamic compromise.1-3
5. Oxygenation: The successful binding of oxygen to hemoglobin at the cellular level in the alveoli, drives SaO2 (arterial oxygen saturation) and SpO2 (oxygen saturation) values. Successful alveolar gas exchange enables efficient aerobic respiration at the cellular level in all perfused body tissues. 1-3
6. Diffusion/exchange: The process where oxygen (O2) is exchanged with CO2 on red blood cells in the alveoli/pulmonary capillaries for transport to body tissues. Pathologic conditions such as pulmonary edema, pneumonia, and acute respiratory distress syndrome (ARDS) can impair diffusion of oxygen across the alveolar membrane leading to reduced oxygen saturation of hemoglobin. 1-3
7. Fraction of Inspired Oxygen (FiO2): Normal atmospheric air contains 21% oxygen or an FiO2 of 0.21. By increasing the percentage of oxygen delivered to the patient (supplemental oxygen), you can potentially increase the arterial oxygen saturation and oxygen content of the bloodstream. 1-3
8. Dead Space: Any part of the airway where gas exchange does not occur, pharynx, larynx, trachea, bronchi, and ventilator tubing are examples.
9. Hypoxia: A state of O2 deficiency in the tissue significant enough to cause impairment of function. Causes can be multifactorial to include low PaO2 due to elevation/altitude(>10,000 feet), decreased available RBCs such as hemorrhage or decreased RBC functionality such as CO poisoning, inadequate circulation or perfusion such as G force pooling or hypotension causes without RBC deficits, and decreased tissue level oxygen transport such as in cyanide poisoning. 1-3