Respiratory 4

Ventilatory muscle power + central respiratory drive must be sufficient to overcome the respiratory load (work of breathing)

Inspiration requires active contraction of the ventilatory muscles

exhalation is passive

major muscle of breathing

Motor innervation is via the phrenic nerve, off the spinal cord at C3, C4, and C5

Contraction INC intraabdominal pressure-->raises the base of the rib cage--> INC rib cage volume--> negative intrathoracic pressure

1. maintain chest wall stability
2. optimize diaphragm function

- innervated by thoracic vertebral nerves

maximum tension a muscle can develop

measured as a pressure gradient across the diaphragm (Pdi = Pab – Ppl)

proportional to cross sectional area of muscle

muscle fibers are shortened --> maximal tension generated by diaphragm DEC

ability to perform work at a certain level, or resistance to fatigue

Muscle fibers produce energy in order to be able to perform work

Muscles with high oxidative capacity can produce more energy -> more resistant to fatigue

when it has to gen more than 40% of its maximal transdiaphragmatic pressure (Pdi) on each breath --> fatigue

Occurs when
1. Respiratory load is too high
2. Diaphragm is too weak

when combined inspiratory muscles have to generate greater than 60% of maximal inspiratory pressure on each breath

Near diaphragm fatigue, subjects switch to breathing predominantly with intercostal and accessory muscles, and vice versa.

Ventilatory muscles alternate back and forth

Hypoxia
Hypercapnia
Acidosis
Malnutrition
Hyperinflation
Infancy
Increased respiratory loads
Disuse

Diaphragm fatigue is a cause of respiratory failure

1. Voluntary or behavioral control of breathing

2. Automatic or metabolic control of breathing

anatomically housed in the cerebral cortex

not tightly regulated by blood gases

responsible for:
1. Voluntary breathing
2. Speech
3. Laughing

anatomically housed in brainstem (medulla)

Breathing is tightly regulated by blood gases

input from many pulmonary reflexes

motor response: sensor, integrator to process the information + motor output

Oxygen and CO2 are sensed by chemoreceptors.

If CO2 is too high, or oxygen too low, these sensors send impulses to the ventilatory controller--> increase breathing

The ventilatory controller
sends information via the phrenic nerve to the diaphragm to increase contraction, and thereby increase VE

1. located in medulla
2. responds to H+ change in CSF
3. CO2 diffusing into the CSF from the blood --> CSF acidosis --> stimulates the chemoreceptors
4. respond to acute changes in PaCO2
5. responsible for the fine- tuning of normal breathing min to min

VE INC linearly with INC PaCO2.

The slope of the line is the Hypercapneic ventilatory response

seperately inc linearly with increasing PaCO2

1. exacerbate the hypercapneic ventilatory response, making the slope steeper

2.inhibit the hypercapneic ventilatory response

inhibit the hypercapneic ventilatory response

1. Located in the Carotid Body at the bifurcation of the internal and external Carotid arteries
2.provide a safety mechanism to stimulate breathing in the face of profound ventilatory crises
3.

Pao2 <60 torr stimulates ventilation via Carotid body stimulation

VE increases exponentially with falling PaO2

VE increases linearly with falling SaO2

defined by slope of SaO2 vs. VE.

Negative slope
VE inc as SaO2 dec

Large increases in Paco2 (>10-20 torr) stimulate ventilation via Carotid body stimulation

Large falls in pH (>0.1-0.2 pH units) stimulate ventilation via Carotid body stimulation

Hyperoxia (Pao2 >~160 torr) inhibits VE. There is a tonic peripheral chemoreceptor stimulation of the ventilatory controller, which contributes to resting ventilation

Hyperoxia will suppress that stimulation, decreasing VE.

alkalosis inhibits the ventilatory response to hypoxia

Stretch receptors inhibit inspiration with increasing lung volume

adapt slowly and steadily to inspiration-->increasing the intensity of neuronal firing (Herring-Breuer reflex)

Afferent information is sent via the Vagus nerve

respond to chemical or mechanical stimulation of irritant receptors in the airway mucosa of large airways

initial burst of neuronal activity in response to inspiration, but this is not sustained.

constricts airways and promotes rapid, shallow breathing--> limits lung penetration of an inhaled substance

also contribute to the initiation of periodic sighs, which occur in normal breathing.

located adjacent to pulmonary capillaries

stimulated by mechanical distortion of connective tissue structure (occurs with pulmonary edema)

Stimulation causes expiratory apnea,then rapid shallow breathing.

Stimulation can cause bronchoconstriction and increased mucous secretion.

Intercostal muscles are rich in muscle spindle fibers (stretch receptors)

These provide proprioception for speech and fine tuning for other voluntary respiratory maneuvers.

Inward distortion of the rib cage during inspiration can stimulate intercostal muscle spindle fibers, which inhibits inspiration.

This intercostal phrenic inhibitory reflex can cause apnea in infants.

Stimulation of breathing occurs with:
fever
pain
alertness
anxiety
fear

Hypoxia DEC brain tissue metabolism--> DEC VE

Hypoxia stimulates peripheral chemoreceptors--> INC VE

this INC in VE --> DEC PaCO2 --> DEC VE by central chemoreceptors

Hypoxia inc cerebral bloodflow--> dilutes PCO2 in brain --> dec VE

Central chemoreceptors respond to dec PCO2 --> DEC VE

Initially, hypoxia (DEC PO2) stimulates VE

INC in VE causes DEC PCO2, INC pH

The DEC PCO2 and INC pH inhibit central chemoreceptors, causing DEC VE

Hypoxic stimulation of VE and DEC PCO2 inhibition alternate to cause periodic breathing

After some time at altitude, CSF [H+] INC, in compensation for the chronic DEC PCO2

This INC VE by central chemoreceptor stimulation, achieving a new INC VE baseline

Periodic breathing diminishes.

Hemoglobin also increases, which increases blood oxygen content

1. NREM sleep

2. REM sleep

deep sleep or slow wave sleep

3 stages

accounts for 80% of the nights for adults

Rapid eye movement

20% of nights for adults

Control of breathing by the Automatic system--> breathing is tightly regulated to blood gases

regular timing and amplitude of breaths

central depression of breathing relative to wakefulness. Thus, there is a slight DEC Po2 and slight INC Pco2 compared to wakefulness.

slight decrease in chest wall stability and in upper airway skeletal muscle tone compared to wakefulness

Control of breathing is primarily by the behavioral or voluntary system--> breathing is not tightly regulated by blood gases (variability in Po2 and Pco2)

irregular timing and amplitude of breath

marked inhibition of skeletal muscle tone--> decreased chest wall stability due to inhibition of intercostal muscle tone.

There is a propensity for obstructive sleep apnea due to inhibition of upper airway skeletal muscle tone

marked hypoxia and hypercapnia

results in DEC Po2 and INC Pco2 compared to wakefulness

not impt for normal but in lung disease where PO@ is already low sleep can cause -> hypoxia and hypercapnia

Both hypoxic and hypercapnic ventilatory responses are inhibited during sleep compared to wakefulness

a general inhibition of skeletal muscle tone, except for the diaphragm and extra-ocular muscles (which move the eyes)

decreased chest wall stability

During inspiration, a negative pressure is generated inside the thorax

When awake, intercostal muscles contract synchronously with the diaphragm to stabilize the chest wall and prevent inward distortion

In REM sleep, no intercostal contraction, so inward distortion of the rib cage occurs--> decreases lung volume--> increase work of breathing in REM sleep.

contractions are decreased, compared to wakefulness

so some complete or partial obstruction of the upper airway may occur during sleep--> snoring.

severe during REM sleep, when skeletal muscle tone is markedly inhibited

not breathing

may be central or obstructive

always occurs during sleep and is releated to repiratory control

occurs when there is no respiratory effort and no airflow

occurs when there is a repiratory effort (diaphragm contraction) but no airflow due to upper airway occlusion

defined as repetitive episodes of upper(extrathoracic) airway obstruction during sleep

cessation of airflow at the nose and mouth with continued respiratory effort

Increased resistance of the upper airway may also cause hypoxia and/or hypercapnia as a consequence of repetitive or persistent partial upper airway obstruction

1. small upper airway (obesity, craniofacial anomalies)

2. when skeletal muscle tone is further inhbited (CNS depressants, alcohol,etc)

OSAS worst in sleep when skeletal muscle tone is dec in REM sleep

--> cause hypoxia and/or hypercapnia

prs regain upper airway tone by waking up

sleep disruption, decreased total amount of sleep, and excessive daytime sleepiness

increasing the size of the upper airway if possible, elimination of CNS depressants, CPAP or BiPAP, or rarely tracheostomy to avoid the obstruction.