CONTROL OF VENTILATION Joanne Simpson. Basic Sub-groups Central Controller EffectorsSensors InputOutput.

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Presentation transcript:

CONTROL OF VENTILATION Joanne Simpson

Basic Sub-groups Central Controller EffectorsSensors InputOutput

Central Controller

Brainstem  Medullary Respiratory Centre Dorsal Respiratory Group (Inspiration) – responsible for basic ventillatory rhythm Expiratory Area – Used for forceful breathing  Apneustic Centre Lower Pons - Impulses from here have excitatory effect on the inspiratory area of the medulla  Pneumotaxic Centre Upper Pons – regulates volume and rate of respiration (fine tuning)

Cortex  Can override the function of the brainstem within limits  Able to voluntarily halve PCO 2 by hyperventillation causing alkalosis  Duration of breath holding limited by many factors. Primarily PO 2 and PCO 2

Other Parts of the Brain The Limbic System and Hypothalamus can alter the pattern of breathing in affective states such as rage and fear

Effectors

 Muscles of the diaphragm  Intercostal Muscles  Abdominal Muscles  Accessory Muscles Co-ordinated action is the responsibility of the central controller.

Sensors

Central Chemoreceptors  Surrounded by brain ECF and respond to changes in H + concentration, ( ↓ [H + ] suppresses ventillation)  Composition of ECF controlled by surrounding CSF, local blood flow and metabolism  Buffering effect, ( ↑ [CO 2 ] means ↑ liberation of H + and resulting hyperventilation)

Peripheral Chemoreceptors  Found in the carotid bodies chiefly  Respond to decreases in PO 2 and pH, and increases in PCO 2  ↓ PO 2 results in ↑ Ventilation  ↓ pH results in ↑ Ventilation

Lung Receptors  Pulmonary Stretch Receptors Stretching of lungs causes firing of receptor and feedback via the vagus ↓ respiratory frequency by ↑ expiration time  Irritant Receptors Stimulated by noxious gases, smoke and cold air. Impulses travel up the vagus causing bronchoconstriction and hyperpnea  J Receptors Respond to chemicals in the lungs. Impulses travel up the vagus and cause rapid, shallow breathing and dyspnoea

Other Receptors  Nose and Upper Airway Receptors Similar to irritant receptors, initiate coughs/sneezes  Joint and Muscle Receptors Impulses from moving limbs are thought to ↑ ventillation in early stages  Gamma System Muscle spindles that sense elongation of the muscle, therfore giving sensation of dyspnoea if a large respiratoy effort is required to move chest wall  Arterial Baroreceptors ↑ Arterial BP may cause hypoventillation / apnoea – converse is true  Pain and Temperature Stimulus may cause hyperventillation

Questions?