1

RSPT 1207 - CARDIOPULMONARY A&P

REGULATION of VENTILATION

Reference & Reading: Egan’s pp. 164-166, 298 - 305

The brain, spinal cord, subsequent nerves and nerve endings compose the Central Nervous System (CNS). The regulation of breathing occurs within the Central Nervous System. The CNS will receive stimuli, asses and make a decision based on the data received and sends command along a motor nerve (neuron) to the muscles of ventilation.

How the CNS receives stimuli:

I.  CHEMORECEPTORS – Specialized nerve structures that “monitor” the oxygen, carbon dioxide, and H+ in the body and send signals to the medulla in the brain to regulate breathing.

a.  Central Chemoreceptors

1.  Located directly on the medulla and are in contact with CSF and not blood.

2.  The blood and CSF are separated by a membrane called the blood-brain barrier. The barrier is relatively impermeable to H+ and HCO3 – ions, but CO2 is very permeable to the blood-brain-barrier.

3.  When CO2 moves across the blood-brain barrier, it goes through the process of hydrolysis:

CO2 + H2O H2CO3 HCO3- + H+

4.  The H+ ions that build in the CSF as a result of hydrolysis stimulate the central chemoreceptors increasing ventilation almost instantly

5.  By increasing ventilation the PaCO2 reduces as will the CO2 levels in the CSF, causing a decrease in ventilation.

6.  Because of this relationship, it can be said that the central chemoreceptors regulate ventilation through the indirect effects of CO2 on the pH level of CSF.

7.  The response of the H+ ions and the central chemoreceptors are quite sensitive and with changes of even 2 mmHg can trigger a change in the rate of breathing.

8.  Over time in the presence of hypercapnia, the central chemoreceptors will become blunted to the increased H+ level.

b.  Peripheral Chemoreceptors

1.  Located high in the neck at the bifurcation of the internal and external carotid arteries, and also on the aortic arch.

2.  Also called carotid and aortic bodies

3.  This group of chemoreceptors are sensitive to :

ü  Decreased PaO2 (less than 60 mmHg)

ü  Increased PaCO2

ü  Decreased pH (acidosis)

4.  Changes in pH must be as large as 0.05 to 0.1 before the peripheral chemoreceptors respond

5.  When the Central Chemoreceptors do not respond to hypercapnia by increasing the minute ventilation, the peripheral chemoreceptors will respond to hypoxemia.

6.  The hypercapnic person will regulate breathing using his hypoxic drive.

II.  Cerebral Cortex – the upper or higher part of the brain becomes involved in the breathing pattern when a person is aware that he is having breathing difficulties

a.  SOB – When a person is aware that he is having trouble breathing this is called Shortness Of Breath or SOB.

1.  It is not just triggered by hypercapnia, or hypoxemia, but also by having increased WOB and fatigue associated with low compliance or increased RAW.

2.  A person who is hypoxic can feel restless, become frightened and may decide to increase his Ve over the automatic response from the medulla

b.  Deliberate Alterations

1.  The breathing pattern may be altered by the higher parts of the brain for actions such as talking, swimming, singing, and other activities.

2.  As soon as the cerebral cortex ends the interference in breathing for the activity the medulla will take over and breathing will become automatic again.

How the CNS processes information:

There are two portions of the lower brain/brainstem that controls ventilation for a person:

I.  Medulla (Oblongata) – It has been found that the main center for the cyclical pattern for breathing occurs in the medulla. During quiet breathing the inspiratory command fires for about 2 seconds and then 3 seconds is allowed for exhalation. On the surface of the medulla are two areas:

a.  Dorsal Respiratory Groups (DRG):

1.  Contain mainly inspiratory neurons that send impulses to the motor nerves of the diaphragm, and external intercostals muscles.

2.  Vagus and glossopharyngeal nerves send sensory impulses to the DRG from the lungs, airways, peripheral chemoreceptors, and joint proprioreceptors.

3.  These impulses modify the basic breathing pattern in the medulla

b.  Ventral Respiratory Groups (VRG):

1.  Located on either side of the medulla and contain inspiratory and expiratory neurons

2.  Inspiratory neurons send impulses via the vagus nerve to laryngeal and pharyngeal muscles to open vocal cords. Also sent impulses to the diaphragm and external intercostals muscles for inspiration

3.  Expiratory neurons send impulses to the internal interscostal and abdominal expiratory muscles for exhalation.

II.  Pons – the word “pon” literally means bridge. The Pons acts as a bridge between the cerebral cortex and the medulla. It is not involved in rhythmic breathing but modifies the output of the medulla.

It takes commands like “I need to swim/talk/ sing” (cerebral cortex)

Into

“Breathe now, hold now” commands (medulla)

There are two groups of neurons in the pons:

1.  Apneustic Center: the function is ill-defined and can only be demonstrated when it is isolated from the pneumotaxic center and vagus nerves. The patient will breath with prolonged inspiratory gasp with few exhalations.

2.  Pneumotaxic Center: controls the “switch-off” point of inspiration or the inspiratory time. Works with the Apneustic Center to control the depth of inspiration. Strong signals increase the RR. Weak signals prolong inspiration and increase Vt.

How the CNS sends commands:

The spinal cord contain the neural pathways for nerve conduction, both sensation and motor impulses. They are along the spinal cord and lie within the protection of the spinal cord.

I.  Sensory Nerves – Nerves that carry impulses only toward the CNS via cranial nerves

a.  Vagus Nerves – sends information to the medulla about breathing reflexes, blood pressure and cardiac activity. It is the only nerve that extends beyond the head and neck region, extending to the thorax and abdomen

b.  Glossopharyngeal Nerves – Sensations of breathing and blood pressure go to the CNS via these cranial nerves.

II.  Motor Nerves – Nerves that carry impulses only away from the CNS

a.  Phrenic Nerves – Breathing commands are sent along the phrenic nerves

i.  There is a right and left phrenic nerve that runs along the mediastinum to sending motor commands to the diaphragms

ii.  These nerves exit the spinal cord between C3 and C5. Severing the spinal cord above C2 will result in complete chest and diaphragm muscle paralysis.

b.  Intercostal Nerves – These nerves enter the muscle groups between T2 and T11 and run along the rib cage.

Breathing Controlled by Reflexes

I.  Hering-Breur Reflex

a.  Generated by stretch receptors located in the airways

b.  When lung inflation stretched these receptors, signals are sent via vagus nerve to stop inspiration

II.  Deflation Reflex

a.  When there is a sudden collapse in the lung, the deflation reflex results in hyperpnea.

b.  Signal is sent via vagus nerve

III.  Head’s Paradoxical Reflex

a.  When the vagus nerve is blocked, hyperinflation of the lung occurs and causes an increase in Ve.

b.  May be related to increased lung volumes during exercise, periodic sighs during quiet breathing and baby’s first breaths.

IV.  Irritant Receptors

a.  Cholinergic Reflex bronchospasm

1.  Vagal sensory nerve fibers located in larger central airways.

2.  Rapidly adaptive

3.  Activated by tactile stimulation

ü  Inhaled irritants – histamine, chemicals, cigarette smoke

ü  Mechanical factors – dust, particulate matter

ü  Pulmonary congestion

4.  Stimulation can result in

ü  Bronchoconstriction

ü  Hyperpnea

ü  Laryngospasm

ü  Glottis closure

ü  Coughing

b.  Vagovagal Reflex

1.  When the reflex has both sensory and motor vagal components

2.  Activated by physical stimulation of conducting airways

ü  Endotracheal intubation

ü  Airway suctioning

ü  Bronchoscopy

3.  Stimulation can result in

ü  bradycardia

ü  coughing

ü  laryngospasm

V.  J Receptors

a.  Also called Juxtacapillary Receptors

b.  Located next to pulmonary capillaries

c.  Activated by

ü  Alveolar inflammatory responses – pneumonia

ü  Pulmonary vascular congestions – CHF

ü  Pulmonary edema

d.  stimulation results in

ü  rapid, shallow breathing

ü  a feeling of dyspnea

ü  narrowing of the glottis on exhalation

Abnormal Breathing Patterns

I.  Cheyne-Stokes Breathing

a.  Ve increases, reaches a “climax,” then decreases then apnea occurs.

b.  A delay is present between the PaCO2 in the CNS, and the PaCO2 in the rest of the body.

c.  Usually caused by a decreased Cardiac Output (CHF) and some brain injuries.

d.  Blood flow is slow between the two areas.

e.  The brain is reacting to the acidotic CSF when the lower arterial CO2 suddenly arrives it causes apnea.

II.  Biot’s Breathing

a.  During regular breathing there is apnea

b.  Similar to Cheyne-Stokes, but the Vt does not change

c.  Caused by increased intracranial pressure

III.  Apneustic Breathing

a.  Caused by damage to the pons.

b.  Persistant Hyperventilation with prolonged inspiratory holds followed by short exhalations

IV.  Central Neurogenic Hypoventilation

a.  Respiratory Centers do not respond to ventilatory stimuli appropriately, i.e. – does not respond to changes in acid-base balance

b.  Associated with head trauma, brain hypoxia, narcotic suppression of respiratory center

V.  Central Neurogenic Hyperventilation

a.  Persistent hyperventilation because the CNS is responding to abnormal stimuli

b.  Related to midbrain and upper pons damage

c.  Associated with head trauma, sever brain hypoxia, and lack of blood flow to brain.