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41 Cards in this Set

  • Front
  • Back

chemoreceptors

look at pO2, pCO2 in teh blood

the controller of ventilation in the brain

the pond and the medulla

medulla

dorsal respiratory group is associated with inspiration; ventral respiratory group is associated with expiration; pre-botzinger complex is the pattern generator also ventrally located in the medulla

pons

apneustic center has an excitatory function; pneumotaxic center can inhibit inspiration

other regions of the brain that affect respiration

cortex which can exercise voluntary control (you can consciously hyperventilate; breath holding is more difficult but you can train to do this consciously); limbic system and hypothalamus that deal with emotional states (excitation or fear)

the effectors that are acted upon by the brain regions we were talking about

diaphragm (innervated by the phrenic nerve), intercostal muscles (mostly inspiration), abdominal muscles (important in active expiration and exercise), accessory muscles in the neck (supported by the first rib)

sensors of breathing issues

central chemoreceptors, peripheral chemoreceptors (2 sets), lung receptors (detect expansion of the lung)

chemoreceptors

specialized tissue that responds to a change in the chemical composition of the blood or other fluid; central chemoreceptor that sense changes in the extracellular fluid of the brain that's important; peripheral chemoreceptor sensing changes in the arterial blood

central chemoreceptors

the cells that make up the central chemoreceptors are imbedded in brain tissue a few mm below the surface; actually if you place some acid directly on this area you can measure a change in ventilation so this area is probably for most of the minute to minute control of ventilation along the day; the central chemoreceptor responds to pH in the extracellular fluid and this is essentially the pH of the cerebral spinal fluid (CSF); the blood brain barrier won't allow H+ or bicarb through but CO2 can diffuse out and into the CSF; an increase in pCO2 will reduce the pH of the CSF and the chemoreceptor is then stimulated; the pH of the CSF is a bit lower than the blood; CSF=7.32 blood=7.4; the buffering ability of the blood is also lower; a change in pCO2 will result in a larger change in pH; pO2 does not directly affect the central chemoreceptor and therefore the chemoreceptor is mostly governed by the pCO2 level and it's change in pH of surrounding fluids

if you hyper of hypo ventilate over a long period of time

pCO2 rises; if the CO2 rises over a long period of time the pH can be restored by the choroid plexus through the use of bicarb; this region of the brain regulates the composition of the CSF; the choroid plexus is like the kidney of the brain

sometimes during resporatory the pCO2

will be increased but the CSF is normal pH; the CSF bicarb can be reduced by the choroid plexus

summary of the central chemoreceptors: responds to

pH of the ECF

summary of the central chemoreceptors: CO2 diffuses across

the blood brain barrier

summary of the central chemoreceptors: normal CSF pH=

7.32

summary of the central chemoreceptors: CSF has little

buffering capacity (due to the low [protein])

summary of central chemoreceptors: CSF bicarb can be controlled by

the choroid plexus

2 sites of peripheral chemoreceptors

carotid body chemoreceptors and aortic body chemoreceptors

carotid body chemoreceptors

at the junction of the carotid artery and very tiny; this is the most important of the 2; info from these receptors goes to the brain via the glossopharyngeal nerve (nerve 9); made up of glomus cells type 1 and 2; responds to arterial pO2 (not really venous pO2); as you lower arterial pO2 (like at high altitude) the response increases rapidly

aortic body receptors

near the aortic arch; info from these receptors communicates through the vagus nerve (cranial nerve 10)

the peripheral chemoreceptors respond to

changes in arterial pO2 but not pH; under normoxic conditions the response to changes in pO2 is very small; the response to changes in pCO2 is slower than for central chemoreceptors; they are the most important receptors causing an increased ventilation in response to a rise in pCO2; they have a high blood flow per gram of tissue

summary of carotid body

responds to pO2, pCO2, and pH (but for the most part only pO2); little response to normoxia; very high blood flow; responds to arterial and not venous pO2; fast response time

lung receptors include

pulmonary stretch receptors, irritant receptors, J receptors (juxta capillary receptors), and bronchial C fibers

pulmonary stretch receptors

this is sometimes called the slowing adapting pulmonary stretch receptors, the output of the receptors remains constant; also responsible for the hering-breuer reflex= if you inflate the lung then you inhibit further inflation

irritant receptors

respond to cigarette smoke, smog, toxic gases, cold air; located in the bronchial walls; stimulation of these causes bronchial constriction; sometimes asthma pts will have an attach after breathing cold air

J receptors

aka juxta capillary receptors; if you inject something in the cap circulation you get a rapid response; they cause rapid shallow breathing; in pulmonary edema fluid leaks out of the caps and into the interstitial space; it can stimulate these receptors; pts with pulmonary edema can become dyspneaic (short of breath); in interstitial fibrosis could also stimulate J receptors; these pts also are often dyspneic

bronchial C fibers

similar to the J receptors except they're supplied by the bronchial circulation

other receptors

nose and upper airway; joint and muscle; gamma system; arterial baroreceptors; arterial baroreceptors; pain and temp

receptors in the nose

similar to the irritant receptors; cold are noxious gas and can cause constriction of airways of the lung

the receptors in the muscles and joints

may have something to do with the increase in ventilation on exercise but this isn't completely understood

gamma system

can sense the elongation of muscles; maybe responsible for the sensation of dyspnea (shortness of breath)

the baroreceptors

for example in space the ventilatory response to pO2 is reduced compared to people at sea level; the baroreceptors in space sense a higher pressure in space due to the lack of hydrostatic pressure of the blood

pain and temp

sudden pain may cause a gasp or period of breath holding

summary: the 2 components of the respiratory control system are

sensors, central controller, and effectors (muscles)

ventilatory response to CO2

there is some interaction/crosstalk between pO2 and pCO2; the level of CO2 in the blood is what controls ventilation

response to CO2

primary factor in ventilation; response is altered by sleep, age, genetic factors, training; reduced by increasing the work of breathing; training- swimmers have a reduced response to CO2; work of breathing- if you ask someone to breathe through a tube (respiratory obstruction) then work of breathing increases and there is a reduced ventilatory response to CO2

ventilatory response to pO2

if you raise pCO2 the response to pO2 increases; again there is an interaction between the 2 sensing systems

response to reduced pO2

no role under normoxic conditions; increased response if the pCO2i s raised; important at high altitude; important in some pts with chronic lung disease

response to reduced pH

sensed by peripheral chemoreceptors; important in metabolic acidosis; if the reduction is severe, central chemoreceptors may be stimulated, under certain circumstances

respnse to exercise

blood gases are normal; pH is normal except in heavy exercise; cortex involvement?; impulses from limbs; increased temp; re setting the CO2 reference levels

sleep apnea

obstructive- very common, often associated with obese individuals; central- respiratory depression during sleep; most common is sleep apnea where tissues in the pharynx relax and fall into the airway; snoring is common response; first described in obese people but non obese people can also be affected by sleep apnea; to distinguish between the 2 types during electromyograms the subject is trying hard to breath against an obstruction but in central sleep apnea there is no muscle response

during exercise ventilation might increase from 5L/min to >100L/min. stimulation of ventilation with exercise works primarily by way of: a. low arterial PO2 b. high arterial PO2 c. low PO2, in mixed venous blood d. low arterial pH e. none of the above

none of the above; it isn't clear why we ventilate faster