In: Anatomy and Physiology
1. Ventilation refers to breathing. Explain the events that cause us to inhale. Include any relevant laws, the role of the pleurae, any muscles that play a role in quiet inspiration, and the collection of neurons in the brain that directly influences the rate and depth of breathing.
Boyle’s law is expressed by the following formula:
P1V1 = P2V2
In this formula, P1 represents the initial pressure and V1 represents the initial volume, whereas the final pressure and volume are represented by P2 and V2, respectively. If the two- and one-liter containers were connected by a tube and the volume of one of the containers were changed, then the gases would move from higher pressure (lower volume) to lower pressure (higher volume).
Diaphragm. The diaphragm is the major muscle responsible for breathing. It is a thin, dome-shaped muscle that separates the abdominal cavity from the thoracic cavity. During inhalation, the diaphragm contracts, so that its center moves caudally (downward) and its edges move cranially (upward).
THE ROLE OF PLEURAE:
The pleural cavity always maintains a negative pressure. During inspiration, its volume expands, and the intrapleural pressure drops. This pressure drop decreases the intrapulmonary pressure as well, expanding the lungs and pulling more air into them.
COLLECTION OF NEURONS IN THE BRAIN THAT INFLUENCE BREATHING:
The neural control of respiration refers to functional interactions between networks of neurons that regulate movements of the lungs, airways and chest wall and abdomen, in order to accomplish (i) effective organismal uptake of oxygen and expulsion of carbon dioxide, airway liquids and irritants, (ii) regulation of blood pH.
Medulla – The primary role of the medulla is regulating our involuntary life sustaining functions such as breathing, swallowing and heart rate. As part of the brain stem, it also helps transfer neural messages to and from the brain and spinal cord.
Recent advances have clarified how the brain detects CO2 to regulate breathing (central respiratory chemoreception). These mechanisms are reviewed and their significance is presented in the general context of CO2/pH homeostasis through breathing. At rest, respiratory chemoreflexes initiated at peripheral and central sites mediate rapid stabilization of arterial PCO2 and pH. Specific brainstem neurons (e.g., retrotrapezoid nucleus, RTN; serotonergic) are activated by PCO2 and stimulate breathing. RTN neurons detect CO2 via intrinsic proton receptors (TASK-2, GPR4), synaptic input from peripheral chemoreceptors and signals from astrocytes. Respiratory chemoreflexes are arousal state-dependent whereas chemoreceptor stimulation produces arousal. When abnormal, these interactions lead to sleep-disordered breathing. During exercise, “central command” and reflexes from exercising muscles produce the breathing stimulation required to maintain arterial PCO2 and pH despite elevated metabolic activity. The neural circuits underlying central command and muscle afferent control of breathing remain elusive and represent a fertile area for future investigation.