Resistance, or frictional forces, associated with ventilation are the result of the anatomical structure of the conductive airways and the tissue viscous resistance of the lungs and adjacent tissues and organs.
 
As the lungs and thorax move during ventilation, the movement and displacement of structures such as the lungs, abdominal organs, rib cage, and diaphragm create resistance to breathing. Tissue resistance remains constant under most circumstances. For example, an obese patient or one with fibrosis has increased tissue resistance, but it usually does not change significantly when these patients are mechanically ventilated. On the other hand, if a patient develops ascites, or fluid build-up in the peritoneal cavity,tissue resistance increases.
 
During mechanical ventilation, resistance of the airways is the factor most often evaluated. The ability of air to flow through the conductive airways depends on the gas viscosity, the gas density, the length and diameter of the tube, and the flow rate of the gas through the tube. In clinical situations, viscosity, density, and tube or airway length remain fairly constant.
 
The diameter of the airway lumen and the flow of gas into the lungs can decrease as a result of bronchospasm, increased secretions, mucosal edema, or kinks in the endotracheal tube. The rate at which gas flows into the lungs can be controlled on most mechanical ventilators.
 
At the end of the expiratory cycle, before the ventilator cycles into inspiration, normally no flow of gas occurs; the alveolar and mouth pressures are equal. Because flow is absent, resistance to flow is also absent. When the ventilator cycles on and creates a positive pressure at the upper airway, the gas attempts to move into the lower pressure zones in the alveoli. However, this movement is impeded or even blocked by having to pass through the endotracheal tube and the upper conductive airways.
 
The relationship of gas flow, pressure, and resistance in the airways is described by the equation for airway resistance:
Raw = P TA /flow
where Raw is airway resistance and P TA is the pressure difference between the mouth and the alveolus, or the transairway pressure. Flow is the gas flow during inspiration. Resistance is usually expressed in centimeters of water per liter per second (cm H2O/L/sec).
 
In normal, conscious individuals with a gas flow of 0.5 L/sec, resistance is about 0.6 to 2.4 cm H2O/L/sec. The actual amount varies over the entire respiratory cycle.
 
With an artificial airway in place, normal airway resistance is increased. The smaller internal diameter of the tube creates greater resistance to flow [resistance can be increased to 5 to 7 cm H2O/(L/sec)]. Diseases of the airway can also increase resistance. In conscious, unintubated subjects with emphysema and asthma, resistance may range from 13 to 18 cm H2O/(L/sec). Still higher values can occur with other severe types of obstructive disorders.
 
With higher resistance, more of the pressure for breathing goes to the airways and not the alveoli. With less pressure in the alveolus, a smaller volume of gas is available for gas exchange.
 
Another disadvantage of high resistance is that more force must be exerted to try to get the gas to flow through the obstructed airways. To achieve this force, spontaneously breathing patients use the accessory muscles to try to breathe in. This generates more negative intrapleural pressures and a greater pressure gradient between the upper airway and the pleural space to achieve gas flow. The same occurs during mechanical ventilation; more pressure is exerted by the ventilator to try to "blow" the air into the patient's lungs through obstructed airways or through a small endotracheal tube.