Lecture 18 Respiration 4 Flashcards
Hypoxia/hypoxemia/dysoxia
Hypoxia - lack of O2 availability in tissues
Hypoxemia- relative deficiency of O2 in blood, arterial PO2 <80mmHg
Dysoxia - Lack of O2 utilisation by tissues
Respiratory diseases
Asthma, cystic fibrosis
COPD - chronic obstructive pulmonary disease- with chronic bronchitis and/or emphysema and epiglottis
Emphysema - walls of air sacs worn away greatly reduced surface area
COPD = chronic bronchitis + emphysema
Chronic bronchitis - inflammation in lungs causes large amount of mucus production.
Increased mucus has 2 effects:
Buildup/ blockage of bronchioles
Breeding ground for bacteria
Emphysema
Persistent coughing causes stiff tissues and structural damage
Less functional alveoli available adding to respiratory issues
Smoking / air quality / hygiene hypothesis
Premature ageing of lungs, stopping smoking will allow longer life even if you stop late in life
Air quality is important, particulate matter from burning fuels also cause airway problems
Hygiene hypothesis - living in over clean conditions increases risk of developing asthma/allergies
respiratory control centre sensors and effectors
Sensors feed into resp centre which acts as a comparator that signals to effectors
Sensors:
Central chemoreceptors: H+
Peripheral chemoreceptors H+, O2, CO2
Pulmonary receptors - stretch
Joint and muscle receptors stretch/tension
Effectors:
Diaphragm
Inspiration - external intercostal and accessory muscles
Expiration - internal intercostals and abdominal muscles
Regulation of ventilation
Breathing, rhythmic, autonomic
Contraction of diaphragm+intercostals initiated by groups of neurones in brain stem
Central pattern generator - intrinsic rhythmic activity
Black box in physiology. model:
1) respiratory neurons in medulla control inspiration+ expiration
2)neurons in pons modulate ventilation
3) rhythmic pattern of breathing arises from network spontaneously discharging neurons
4) ventilation modulated by chemical factors+ higher brain centres
Medulla oblongata controlled basic breathing rhythm
2 discrete cell groups in the medulla oblongata
Dorsal respiratory group (DRG)
Dorsal location in the nucleus tractus solitarius (NTS) neurons active during inspiration - controls diaphragm and intercostal muscles
Ventral respiratory group (VRG) nucleus ambiguus (N/a) inspiratory and expiratory related neurons - for active expiration and greater than normal inspiration - used for vigorous exercise
Inputs via vagus nerves alter DRG and VRG activity
Inputs via vagus nerve and higher brain centres alter DRG/VRG activity
Inspiratory neurones in VRG and DRG project via motor neurones to the cervical region spinal cord
Motor neurone axons (phrenic+ intercostal) link to inspiratory muscles to breathe in or out
Inhibition/off switchon expiration
Neural activity during quiet breathing
During inspiration the activity of inspiratory neurons increases steadily apparently through a positive feedback mechanism. At the end of inspiration, the activity shuts off abruptly and expiration takes place through recoil of elastic lung tissue
CO2, O2 and pH influence ventilation
Chemoreceptors monitor partial pressure PO2 and PCO2
Peripheral - carotid and aortic bodies respond to decreased arterial PO2 and especially PO2 & H+ ions
Central nervous system receptors in ventral surface medulla
Differ in structure/location and chemical sensitivities
Pulmonary stretch receptors influence too
Herring Browser inflation reflex
Determines rate and depth of breath. Observed in anaesthetised dogs that if tidal volume exceeded a certain volume then stretch receptors in the lungs signal to brain stem to terminate inspiration
Peripheral chemoreceptors
Type l and type ll cells
Type l - contract blood communicate via afferent nerves- neurotransmitter
Type ll - “glial cell like” repair+ nutrient supply
Stimuli PO2 (hypoxia) and pH (PCO2 change)
PO2 drops below 60mmHg before significant breathing change
Dissociation curve 60mm Hg blood still 90% saturated O2 content high
H+ ions (pH) primary stimuli
H+ ions formed by CO2+H20
PCO2 stimuli indirect
Central chemoreceptors
Neurons on ventral surface medulla
H+ ions stimuli pH change in cerebrospinal fluid
H+ do not cross brain blood barrier but CO2 does
CO2 > H+ + H2CO3- (carbonic anhydrase in cerebrospinal fluid)
Chemoreceptor reflex
Central+ peripheral primary respond to changes in PCO2 (increase causes inhalation)
Peripheral -pH arterial blood
Peripheral -PO2 effect only when O2 drops to low levels
Activation of chemoreceptors causes increased ventilation
Decrease in activation leads to decreased ventilation
Chemoreceptor reflex
Sea level PO2= 160mm Hg
PCO2= 0.2mmHg
Alveolar+arterial PO2 = 100mmHg
PCO2= 40mm Hg
As long as ventilation matches metabolic demands on body
Hypoventilate:
Arterial PCO2 up and PO2 down
PCO2 stimulates chemoreceptors to increase breathing rate + depth
PO2 only a stimulus in severe hypov
Hyperventilation:
Arterial PO2 up and PCO2 down
Chemoreceptor stimulation reduced
(Lack of PCO2) decrease in breathing rate+ depth
