respiratory phys 7 Flashcards

1
Q

what is spontaneous respiration regulated by? how is THAT controlled?

A
  • spontaneous respiration is regulated by rhythmic discharges coming from motor neurons from the pons and medulla that are controlled by chemical control and changes in arterial PO2 and PCO2 and H+ concentrations
  • can also be supplemented by nonchemical influences
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2
Q

where is the voluntary respiratory control system

A

in the cerebral cortex

sends impulses to respiratory motor neurons located in spinal cord via the cortico-spinal tracts

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3
Q

why do we not inhale and exhale at the same time

A

the expiratory muscles are inhibited when those supplying the inspiratory muscles are active and vice-versa

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4
Q

walk through the steps of where the signal goes thru when there is a change in oxygen or CO2 or pH. what is an exception to this pathway?

A
  • sent to PERIPHERAL chemo-receptors
  • sent to sensory integration
  • sent to central pattern generator
  • out to spinal cord
  • then to respiratory muscles and out to chest wall, diaphragm, conducting airways to increase ventilation

-> exception to this pathway is when there’s a large CO2 increase and that signal gets sent straight to central chemo receptors that goes to the CENTRAL pattern generator

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5
Q

What is the main controller of respiration? what are it’s properties in the body

A
  • pCO2 is the major controller of respiration
  • high colubility and no Hgb buffer
  • acute increases in pCO2 have a stronger effect than decreases in pH
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6
Q

WHAT CAN INCREASE PO2?

A
  • normally, an increase in CO2 causes an increase in O2 however, in the absence of CO2, O2 is increased anyway with the decrease in O2 via the PERIPHERAL CHEMORECEPTOR
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7
Q

when is the peripheral chemoreceptor system particularly sensitive to changes in arterial PO2?

A
  • from 60-30 mmHg

- this is a range in which Hgb saturation with oxygen decreases rapidly

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8
Q

what effect does H have on chemoreceptors and why

A

H stimulates the chemosensitive area but CO2 in the fluid give rise to most of the H

  • > how? when there is CO2, it conjugates with H2o and enters the blood brain barrier to dissociate as bicarb and H+
    reason: since H does not easily cross the blood brain barrier, it changes in blood H have considerably less effect in stimulating the chemosensitive neurons than do changes in blood CO2
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9
Q

what are the main peripheral chemoreceptors? what do they respond to the most? secondarily?

A

aortic and carotid bodies

-respond to changes in O2 first but also respond to a lesser extend to CO2 ad pH (H)

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10
Q

what are the main central chemoreceptors? what do they respond to

A
  • they are located in the ventral lateral medullary surface as the 1) rostrel area 2) intermediate area 3) caudal area
  • sensitive to H and PCO2
  • in turn excites other portions of the respiratory center
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11
Q

what is the sensory integration system?

A

-it is where all the chemoreceptors and baroreceptors come together on the respiratory center

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12
Q

what are the four main neurons that are in the respiratory center

A
  • DRG- dorsal respiratory group-
  • PRG- pneumotaxic respiratory group
  • Ventral respiratory group pre- botzinger complex
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13
Q

what is the pre botzinger complex

A
  • pacemaker cells that initiate rhythmic respiration

- on both sides of the medulla between the nucleus ambiguous and lateral reticular nucleus

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14
Q

what is the dorsal respiratory group

A
  • sends out repetitive bursts of inspiratory neuronal action potentials (inspiratory ramp signals)
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15
Q

what is the pneumotaxic center?

A
  • it’s located in the nucleus parabrachialis of the upper pons
  • transmits signals to the inspiratory area (DRG) and decreases activity of DRG and inspiration to allow for expiration
  • control the switch- off point of the inspiratory ramp
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16
Q

what does the ventral respiratory group do?

A
  • located in each side of the medulla
  • TOTALLY INACTIVE DURING NORMAL QUIET RESPIRATION
  • when need more pulmonary ventilation, respiratory signals spill over to the ventral group from the DRG (DRG -> VRG)
  • contributes to BOTH INSPIRATION AND EXPIRATION
  • VERY IMPORTANT IN PROVIDING POWERFUL EXPIRATORY SIGNALS TO THE ABDOMEN MUSCLES DURING HEAVY EXPIRATION
17
Q

during exercise, what occurs with CO2 and O2 and pH in a normal person? how is this done?

A
  • they all stay relatively normal as the oxygen demands are met with ventilation
  • maintained thru the use of the brain!! just as the brain is sending signals to the motor neurons in the muscles, it also is sending collateral signals to the respiratory center of the brain stem
18
Q

what are irritant receptors

A
  • can effect breathing too:
  • they are located at the epithelium of trachea, bronchi and bronchioles
  • activated by bronchial edema or inhalation of toxic substances
  • cause coughing and sneezing but also can cause bronchial constriction in asthma and emphysema
19
Q

what are J receptors

A
  • sensory nerve endings in the alveolar walls facing the interstitium which makes them sensitive to changes in the interstitium -like when capillaries have edema
  • give a feeling of dyspnea
20
Q

what does brain edema cause? what helps

A
  • activity in the respiratory center maybe depressed or even inactivated by acute brain edema resulting from concussion => no breathing!
  • mannitol aka hypertonic solution helps
21
Q

stretch receptors -the hering breuer inflation reflex

A
  • receptors located in muscular portions of bronchi and bronchioles
  • transmit signals thru the vagi into the dorsal root ganglion when the lungs are OVERSTRETCHED
  • activate signals that are switched off in the inspiratory ramp and THUS STOP INSPIRATION
  • INCREASES RATE OF RESPIRATION
  • NOT ACTIVATED UNTIL TENSION > 3TIMES NORMAL VALUE
  • PROTECTIVE- for preventing excess lung inflation
22
Q

kaussmaul’s breathing

A

relentless, rapid and deep

AIR HUNGER - DUE TO METABOLIC ACIDOSIS

23
Q

cheyne-stokes breathing

A

ventilatory oscillation with long cycle times found in -strokes, encephalopathies and HF
-also has periods of apnea

24
Q

Biots breathing

A
  • groups of quick, shallow inspirations followed by regular or irregular periods of apnea-totally messed up mannnnnn!
  • found in medullary trauma, stroke
25
Q

what are the three types of pulmonary disorders? examples

A

1) obstruction from conditions in the wall lumen -asthma, acute/chronic bronchitis
2) obstruction related to loss of lung parenchema- emphysema
3) obstruction of the airway of the lumen- bronchiectasis, bronchiolitis, CF, Epiglottitis, croup

26
Q

what are the key features when it comes to asthma, bronchitis and emphysema?

A

asthma- high reversibility and low alveolar damage
chronic bronchitis- hi sputum, medium reversibility, medium alveolar damage
emphysema- low reversibility moderate sputum, lots of alveolar damage

27
Q

asthma

A
  • hi reactivity of airways to stimuli
  • diffuse airway inflammation
  • 2 types- allergic (extrinsic-pediatric onset) and non allergic (intrinsic-adult onset)
28
Q

characteristics of extrinsic asthma

A
  • pediatric onset
  • usually has genetic predisposition for smaller airways (chrom 5, 11, 14)
  • fam hx of hay fever or eczema
  • pos skin test to allergens
29
Q

characteristics of intrinsic asthma

A
  • non- allergic, adult onset
  • develop middle age
  • no hx of allergy
  • respiratory infection or psychological factors contribute
  • antigen-antibody reactions have a lesser role
  • allergen specific immunotherapy and environmental control measures not helpful
  • less favorable prognosis
30
Q

pathophysiology of asthma

A

1) allergen irritates epithelium and causes release of inflammatory cytokines
2) inflammatory cytokines/mediators cause epithelial shedding, sub epithelial fibrosis, plasma leakage and edema, vasodilation and angiogenesis, parasympathetic nerve activation (BRONCHOCONSTRICTION) and plasticity and also causes mucus production
3) since mucus is secreted but epithelium is gone, there is a blockage of mucus

31
Q

What are the 4 main results of asthma

A

1) increased secretions
2) accumulation of cellular debris from epithelial damage and airway inflammation
3) SM contraction and hyperplasia and hypertrophy
4) submucosal thickening by edema and infiltration

32
Q

what do you see on a physical examination of a pt having an asthma attack?

A
  • rapid breathing
  • tachycardia
  • pulsus paradoxus- when inspire, pulse pressure decreases
33
Q

what do you see in the thoracic examination of a pt having an asthma attack

A
  • accessory muscles of ventilation are used
  • expiratory&raquo_space;> inspiratory
  • hyperinflated chest
  • hyperresonance/ percussion
  • WHEEZING