BY RONALD OMBAKA ESQ.

CONTROL OF RESPIRATION

Goal:

maintain sufficient ventilation with minimal energy

The three basic elements of the respiratory control system are

1.Sensors that gather information

2.Central controller in the brain, which coordinates the information 3.Effectors(respiratory muscles), which cause ventilation.

The central controller:

Brian stem

The periodic nature of inspiration and expiration is controlled by the central pattern generator that comprises groups of neurons located in the pons and medulla.

These groups are;

Medullary respiratory center- in a region called the Pre-Botzinger Complex( Dorsal and ventral resp. group)

Apneustic center in the lower pons.

Pneumotaxic center in the upper pons. This area“switchs off” or inhibits inspiration and thus regulate inspiration volume and, secondarily, respiratory rate.

Ultimately the central controller

Receives input from chemoreceptors, lung and other receptors, and the cortex.

Generates the rhythmic pattern of inspiration and expiration.

Major output is to the phrenic nerves, but there are also impulses to other respiratory muscles.

(It is an example of a negative feedback loop system)

The Cortex

the cortex can override the function of the brainstem, turning resp. into a voluntary process,though within limits.

Other Parts of the Brain

the limbic system and hypothalamus, can alter the pattern of breathing, for example, in emotional states such as rage and fear.

Effectors:

The muscles of respiration include the

diaphragm,

intercostal muscles,

abdominal muscles,

accessory muscles such as the sternomastoids.

Sensors: Central Chemoreceptors

A chemoreceptor is a receptor that responds to a change in the chemical composition of the blood or other fluid around it.

Central chemoreceptors in the medulla govern minute by minute control of respiration.

The central chemoreceptors are surrounded by brain extracellular fluid and respond to changes in its H+ concentration. An increase in H+ concentration stimulates ventilation, whereas a decrease inhibits it.

Blood is separated from CSF by BBB, H+ & HCO3-are impermeable at the BBB.

Therefore it is CO2 that diffuses from the blood into CSF to yield H+ within the CNS thus stimulating chemoreceptors.

Thus, the CO2 level in blood regulates ventilation chiefly by its effect on the pH of the CSF. (resulting in hyperventilation to reduce CO2)

Sensitive to the PCO2 but not PO2 of blood.

Peripheral Chemoreceptors

Carotid bodies

Aortic bodies

The carotid bodies are the most important in humans.

Contain glomus cells –Type I &II

Respond to decreases in arterial Po2 and pH, and increases in arterial Pco2.

They are sensitive to PO2 drops from 66Kpa max firing occurs at 13kpa

The peripheral chemoreceptors are responsible for all the increase of ventilation that occurs in humans in response to arterial hypoxemia.

The response of the peripheral chemoreceptors to arterial Pco2 is less important than that of the central chemoreceptors.

Increases in chemoreceptor activity in response to decreases in arterial Po2 are potentiated by increases in Pco2 and, in the carotid bodies, by decreases in pH.

Lung Receptors

Pulmonary Stretch Receptors-They discharge in response to distension of the lung. The impulses travel in the vagusnerve.

The main reflex effect of stimulating these receptors is a slowing of respiratory frequency due to an increase in expiratory time.(Hering-Breuer inflation reflex)

Irritant Receptors-lie between airway epithelial cells.

stimulated by noxious gases, cigarette smoke, inhaled dusts, and cold air.

The impulses travel up the vagus and the reflex effects include bronchoconstriction and hyperpnea.

J Receptors-are believed to be in the alveolar walls, close to the capillaries.

They respond very quickly to chemicals injected into the pulmonary circulation.

Can result in rapid, shallow breathing, although intense stimulation causes apnea.

There is evidence that engorgement of pulmonary capillaries and increases in the interstitial fluid volume of the alveolar wall activatethese receptors. They may play a role in the rapid, shallow breathing and dyspnea (sensation of difficulty in breathing) associated with left heart failure and interstitial lung disease.

Bronchial C Fibers –limited to bronchi and respond similarly to J receptors.

Other auxilliary receptors;

Nose and Upper Airway Receptors

Joint and Muscle Receptors

Gamma System

Arterial Baroreceptors

Pain and Temperature

Integrated Responses: Response to Carbon Dioxide

Arterial PCO2 is the most important stimulus to ventilation under most conditions and is normally tightly controlled.

Ventilation increases by about 2 to 3 liters·min−1 for each 1 mm Hg rise in Pco2.(The response is magnified if the arterial PO2is lowered)

A reduction in arterial Pco2 is very effective in reducing the stimulus to ventilation.(An anesthetized patient will frequently stop breathing for a minute or so if overventilatedby the anesthesiologist.)

Trained athletes and divers tend to have a low CO2sensitivity.

Various drugs depress the respiratory center, including morphine and barbiturates.

Patients who have taken an overdose of one of these drugs often have marked hypoventilation.

Response to Oxygen:

the alveolar Po2 can be reduced to the vicinity of 50 mm Hg before any appreciable increase in ventilation occurs.(Concomittant increases in PCO2 augment the ventilatory response)

In some patients with severe lung disease, the hypoxic drive to ventilation becomes very important. These patients have chronic CO2 retention, and the pH of their brain extracellular fluid has returned to near normal in spite of a raised Pco2.(Think COPD)

Response to pH;

A reduction in arterial blood pH stimulates ventilation.

Response to Exercise;

Fit young people who attain a maximum O2 con-sumption of 4 liters.min–1 may have a total ventilation of 120 liters.min–1,that is, about 15 times their resting level.

This increase in ventilation closely matches the increase in O2 uptake and CO2 output.