Thecontrol of ventilation is thephysiological mechanisms involved in the control ofbreathing, which is the movement of air into and out of the lungs. Ventilation facilitates respiration. Respiration refers to the utilization ofoxygen and balancing ofcarbon dioxide by the body as a whole, or by individual cells incellular respiration.[1]
The most important function of breathing is the supplying of oxygen to the body and balancing of the carbon dioxide levels. Under most conditions, thepartial pressure of carbon dioxide (PCO2), or concentration of carbon dioxide, controls therespiratory rate.
Theperipheral chemoreceptors that detect changes in thelevels of oxygen and carbon dioxide are located in thearterialaortic bodies and thecarotid bodies.[2]Central chemoreceptors are primarily sensitive to changes in thepH of theblood, (resulting from changes in the levels of carbon dioxide) and they are located on themedulla oblongata near to themedullar respiratory groups of therespiratory center.[3]Information from the peripheral chemoreceptors is conveyed along nerves to the respiratory groups of the respiratory center. There are four respiratory groups, two in the medulla and two in thepons.[2] The two groups in the pons are known as thepontine respiratory group.
From the respiratory center, themuscles of respiration, in particular thediaphragm,[4] are activated to cause air to move in and out of the lungs.
Breathing is normally an unconscious, involuntary, automatic process. The pattern of motor stimuli during breathing can be divided into aninhalation stage and anexhalation stage.Inhalation shows a sudden, ramped increase in motor discharge to therespiratory muscles (and thepharyngeal constrictor muscles).[5] Before the end of inhalation, there is a decline in, and end of motor discharge.Exhalation is usually silent, except at highrespiratory rates.
Therespiratory centre in the medulla and pons of the brainstem controls the rate and depth of respiration, (therespiratory rhythm), through various inputs. These include signals from the peripheral chemoreceptors and central chemoreceptors; from the vagus nerve and glossopharyngeal nerve carrying input from thepulmonary stretch receptors, and other mechanoreceptors in thelungs.[3][6] as well as signals from thecerebral cortex andhypothalamus.
Ventilation is normally unconscious and automatic, but can be overridden byconscious alternative patterns.[3] Thus the emotions can cause yawning, laughing, sighing (etc.), social communication causes speech, song and whistling, while entirely voluntary overrides are used to blow out candles, and breath holding (for instance, to swim underwater).Hyperventilation may be entirely voluntary or in response to emotional agitation or anxiety, when it can cause the distressinghyperventilation syndrome. The voluntary control can also influence other functions such as theheart rate as inyoga practices andmeditation.[7]
The ventilatory pattern is also temporarily modified by complex reflexes such as sneezing, straining, burping, coughing and vomiting.
Ventilatory rate (respiratory minute volume) is tightly controlled and determined primarily by blood levels ofcarbon dioxide as determined bymetabolic rate. Blood levels ofoxygen become important inhypoxia. These levels are sensed bycentral chemoreceptors on the surface of themedulla oblongata for decreased pH (indirectly from the increase of carbon dioxide incerebrospinal fluid), and theperipheral chemoreceptors in the arterial blood for oxygen and carbon dioxide. Afferent neurons from the peripheral chemoreceptors are via theglossopharyngeal nerve (CN IX) and thevagus nerve (CN X).
The concentration ofcarbon dioxide (CO2) rises in the blood when the metabolic use of oxygen (O2), and the production of CO2 is increased during, for example, exercise. The CO2 in the blood is transported largely as bicarbonate (HCO3−) ions, by conversion first tocarbonic acid (H2CO3), by the enzymecarbonic anhydrase, and then by disassociation of this acid to H+ and HCO3−. Build-up of CO2 therefore causes an equivalent build-up of the disassociated hydrogen ions, which, by definition, decreases the pH of the blood. The pH sensors on the brain stem immediately respond to this fall in pH, causing the respiratory center to increase the rate and depth ofbreathing. The consequence is that thepartial pressure of CO2 (PCO2) does not change from rest going into exercise. During very short-term bouts of intense exercise the release of lactic acid into the blood by the exercising muscles causes a fall in the blood plasma pH, independently of the rise in the PCO2, and this will stimulate pulmonary ventilation sufficiently to keep theblood pH constant at the expense of a lowered PCO2.
Mechanical stimulation of the lungs can trigger certain reflexes as discovered in animal studies. In humans, these seem to be more important in neonates and ventilated patients, but of little relevance in health. The tone of respiratory muscle is believed to be modulated bymuscle spindles via a reflex arc involving the spinal cord.
Drugs can greatly influence the rate of respiration.Opioids andanesthetics tend to depress ventilation, by decreasing the normal response to raisedcarbon dioxide levels in the arterial blood. Stimulants such asamphetamines can causehyperventilation.
Pregnancy tends to increase ventilation (lowering plasma carbon dioxide tension below normal values). This is due to increasedprogesterone levels and results in enhanced gas exchange in theplacenta.
Receptors play important roles in the regulation of respiration and include thecentral andperipheral chemoreceptors, andpulmonary stretch receptors, a type ofmechanoreceptor.