How is respiratory rate regulated

The result is that the excess CO2 is blown out of the lungs. When arterial CO2 levels are abnormally low hypocapnia , respirations become shallow and slow hypoventilation and periods of apnoea may occur as the stimulus to breathe is absent. This reaction can occur as a result of a panic attack and can usually be rectified by rebreathing into a paper bag. Rebreathing expired CO2 leads to a rise in arterial CO2 levels which triggers the chemoreceptor response. A fall in the pH of CSF can be triggered not only by respiratory changes but by metabolic causes.

Typical causes of metabolic acidosis are poorly controlled diabetes mellitus, which allows organic acids to build up, or the increased production and accumulation of lactic acid during exercise.

Whether the cause of the reduction of pH in the CSF is respiratory or metabolic, the central chemoreceptors will be stimulated. The body will react in an attempt to rid itself of excess acids and raise the pH by eliminating CO2 via the lungs.

Peripheral chemoreceptors, bathed as they are in newly oxygenated blood, are sensitive to arterial O2 levels. While they are involved in the response to increased acidity rise in arterial partial pressure of CO2, fall in pH they also respond to falls in the arterial partial pressure of oxygen PO2. There are vast reserves of arterial oxygen bound to haemoglobin in the blood Richardson, , and a large fall in PO2 is needed before these begin to be depleted and the peripheral chemoreceptors are stimulated.

Neuronal messages via the glossopharyngeal nerves from carotid receptors and the vagus nerve from the aortic receptors , stimulate the medullary inspiratory neurones. Rate and depth of respiration are increased and more O2 is inhaled and absorbed into the blood. Once arterial O2 levels return to normal, the stimulus ceases. These peripheral receptors assume a vital importance in patients who retain CO2 due to pulmonary disease such as emphysema or chronic bronchitis. In these patients, the central chemoreceptors become unresponsive to the constant stimulus of CO2 and the peripheral chemoreceptors assume the function of driving respiration the hypoxic drive.

These patients will only breathe when arterial PO2 is low enough to trigger the peripheral chemoreceptors. It is essential that nurses understand this physiological alteration as giving high doses of oxygen therapy to these patients will stop them breathing because O2 levels do not fall low enough to stimulate respiration. Hormones are not only involved in the transmission of nerve impulses within the respiratory system, but recent work suggests that many are involved in the control of respiration Saaresranta and Polo, Progesterone and thyroxine, for example, are known to stimulate respiration, while somostatin and dopamine have a depressant effect.

Many different drugs affect our respiratory rate. Barbiturates, alcohol, anaesthetics and opiates have a depressant effect, while stimulants such as caffeine and amphetamines increase respiratory rate.

A variety of mechanisms are involved and readers are referred to specialist respiratory pharmacology texts. The simple act of breathing in and out is regulated by numerous physiological mechanisms Fig 2. This complicated system enables us to adjust our respirations with great precision, ensuring that every cell in the body receives a constant supply of oxygen and has a means of ridding itself of waste products.

Sign in or Register a new account to join the discussion. You are here: Respiratory. A person with severe diarrhea loses a lot of bicarbonate in the intestinal tract, which decreases bicarbonate levels in the plasma.

As bicarbonate levels decrease while hydrogen ion concentrations stays the same, blood pH will decrease as bicarbonate is a buffer and become more acidic. In cases of acidosis, feedback will increase ventilation to remove more carbon dioxide to reduce the hydrogen ion concentration. Conversely, vomiting removes hydrogen ions from the body as the stomach contents are acidic , which will cause decreased ventilation to correct alkalosis.

Chemoreceptor feedback also adjusts for oxygen levels to prevent hypoxia, though only the peripheral chemoreceptors sense oxygen levels. In cases where oxygen intake is too low, feedback increases ventilation to increase oxygen intake. A more detailed example would be that if a person breathes through a long tube such as a snorkeling mask and has increased amounts of dead space, feedback will increase ventilation.

Respiratory feedback : The chemoreceptors are the sensors for blood pH, the medulla and pons form the integrating center, and the respiratory muscles are the effector. Learning Objectives Describe the role of chemoreceptors in the regulation of breathing. In response to a decrease in blood pH, the respiratory center in the medulla sends nervous impulses to the external intercostal muscles and the diaphragm, to increase the breathing rate and the volume of the lungs during inhalation.

Hyperventilation causes alakalosis, which causes a feedback response of decreased ventilation to increase carbon dioxide , while hypoventilation causes acidosis, which causes a feedback response of increased ventilation to remove carbon dioxide. Respiratory feedback : The chemoreceptors are the sensors for blood pH, the medulla and pons form the integrating center, and the respiratory muscles are the effector.

Evaluate the effect of proprioception the sense of the relative position of the body and effort being employed in movement on breathing. The lungs are a highly elastic organ capable of expanding to a much larger volume during inflation. While the volume of the lungs is proportional to the pressure of the pleural cavity as it expands and contracts during breathing, there is a risk of over-inflation of the lungs if inspiration becomes too deep for too long.

Physiological mechanisms exist to prevent over-inflation of the lungs. Cardiac and respiratory branches of the vagus nerve : The vagus nerve is the neural pathway for stretch receptor regulation of breathing.

The Hering—Breuer reflex also called the inflation reflex is triggered to prevent over-inflation of the lungs. There are many stretch receptors in the lungs, particularly within the pleura and the smooth muscles of the bronchi and bronchioles, that activate when the lungs have inflated to their ideal maximum point.

These stretch receptors are mechanoreceptors, which are a type of sensory receptor that specifically detects mechanical pressure, distortion, and stretch, and are found in many parts of the human body, especially the lungs, stomach, and skin. They do not detect fine-touch information like most sensory receptors in the human body, but they do create a feeling of tension or fullness when activated, especially in the lungs or stomach.

When the lungs are inflated to their maximum volume during inspiration, the pulmonary stretch receptors send an action potential signal to the medulla and pons in the brain through the vagus nerve. This is called the inflation reflex. As inspiration stops, expiration begins and the lung begins to deflate. As the lungs deflate the stretch receptors are deactivated and compression receptors called proprioreceptors may be activated so the inhibitory signals stop and inhalation can begin again—this is called the deflation reflex.

Early physiologists believed this reflex played a major role in establishing the rate and depth of breathing in humans. While this may be true for most animals, it is not the case for most adult humans at rest. However, the reflex may determine the breathing rate and depth in newborns and in adult humans when tidal volume is more than 1 L, such as when exercising. Additionally, people with emphysema have an impaired Hering—Bauer reflex due to a loss of pulmonary stretch receptors from the destruction of lung tissue, so their lungs can over-inflate as well as collapse, which contributes to shortness of breath.

As the Hering—Bauer reflex uses the vagus nerve as its neural pathway, it also has a few cardiovascular system effects because the vagus nerve also innervates the heart. During stretch receptor activation, the inhibitory signal that travels through the vagus nerve is also sent to the sinus-atrial node of the heart. Its stimulation causes a short-term increase in resting heart rate, which is called tachycardia. The heart rate returns to normal during expiration when the stretch receptors are deactivated.

When this process is cyclical it is called a sinus arrhythmia, which is a generally normal physiological phenomenon in which there is short-term tachycardia during inspiration. Sinus arryhthmias do not occur in everyone, and are more common in youth. The sensitivity of the sinus-atrial node to the inflation reflex is lost over time, so sinus arryhthmias are less common in older people. Privacy Policy. Skip to main content. Respiratory System.

Search for:. Respiration Control. Neural Mechanisms Respiratory Center The medulla and the pons are involved in the regulation of the ventilatory pattern of respiration. Learning Objectives Describe the neural mechanism of the respiratory center in respiration control. Key Takeaways Key Points The ventral respiratory group controls voluntary forced exhalation and acts to increase the force of inspiration.

The dorsal respiratory group nucleus tractus solitarius controls mostly inspiratory movements and their timing. Ventilatory rate minute volume is tightly controlled and determined primarily by blood levels of carbon dioxide as determined by metabolic rate.

Chemoreceptors can detect changes in blood pH that require changes in involuntary respiration to correct. The apneustic stimulating and pnuemotaxic limiting centers of the pons work together to control rate of breathing. The medulla sends signals to the muscles that initiate inspiration and expiration and controls nonrespiratory air movement reflexes, like coughing and sneezing.

Key Terms respiratory control centers : The medulla which sends signals to the muscles involved in breathing, and the pons which controls the rate of breathing. The Medulla The medulla oblongata is the primary respiratory control center.

There are two regions in the medulla that control respiration: The ventral respiratory group stimulates expiratory movements. The dorsal respiratory group stimulates inspiratory movements. The Pons The pons is the other respiratory center and is located underneath the medulla. It has two main functional regions that perform this role: The apneustic center sends signals for inspiration for long and deep breaths.

It controls the intensity of breathing and is inhibited by the stretch receptors of the pulmonary muscles at maximum depth of inspiration, or by signals from the pnuemotaxic center.