56: Control of Respiration Flashcards
Central Controller
Pons, medulla, other parts of brain
Effectors
Respiratory muscles, diaphragm, intercoastals
Sensors
Chemo and mechanoreceptors, muscle proprioceptors
What are the three respiratory centers in the Medulla Oblongata?
DRG – dorsal resp. group
VRG – ventral resp. group
PRG - Pontine resp. group
Dorsal Resp. Group
control muscles during inspiration
Output via the
phrenic nerves and intercostal nerves
Receives sensory info from
peripheral chemo and mechanoreceptors
through cranial nerves IX and X
Ventral Resp. Group
active expiration or for greater than normal
inspiration
pre-Botzinger complex
spontaneously firing
neurons, may act as the pacemaker
Pontine Resp. Group
tonic input to medulla to control smooth resp. rhythm
Latent period
after expiration – then a ramp pattern develops
increase action potentials, increase in diaphragm muscle tone, action potential reach max diaphragm muscle tone, action potential cease and diaphragm relaxes
Sensors 1: central
chemoreceptors
ventral surface of the medulla
Responds to a change in PCO2 and pH of (CSF)
CSF
separated from the blood by the BBB – which is largely impermeable to
H+ and HCO3-
Does metabolic acidosis or alkalosis affect CSF pH?
little effect of CSF pH
What is the BBB very permeable to?
O2 and CO2
PCO2 has a strong
effect on CSF pH
raising PCO2, large decrease in CSF pH
Sensors 2: peripheral
chemoreceptors
located in carotid and aortic bodies
Detect changes in PCO2, PO2 and pH
Carotid body
small sensory organ at carotid artery, signals to CNS via the glossopharyngeal
nerves
detect ↓PO2 (below 100 mmHg) and pH
changes
Aortic bodies
multiple bodies along aorta
afferents feed CNS via vagus nerve
Glomus cells
site of chemoreception
↓PO2 – depolarizes glomus cell and
stimulates afferents to the CNS
↑PCO2 in the cells causes acidification – also causes depolarization
H+- causes acid loading into cell - depolarization
Integrated response
Central chemoreceptors primarily involved
but peripheral chemoreceptors also help and respond faster
What is the most important stimulus to ventilatory drive?
PCO2 of arterial blood
When PO2 low
PCO2 is high
Cerebrum
voluntary control
Medulla oblongata
site of dorsal respiratory
center and ventral respiratory center
generate
the basic rhythmic pattern of breathing
Pons
apneustic and pneumotaxic centers can
modulate the basic pattern of the medulla but
are not essential
limbic system and
hypothalamus
Emotional responses
anxiety, rage, fear
Pulmonary Stretch Receptors
in smooth muscle layer of airways
fire in response to transmural pressure
Cause excitation of inspiratory offswitch
& prolongs expiration
Irritant Receptors
in airway epithelium
Respond to touch, noxious substances (smoke or particles) or lung edema
stimulated by histamines, serotonins and prostaglandins (inflammation)
results in coughing/gasping
Juxtapulmonary capillary Receptors
AKA C-fiber endings
Alveolar and bronchial groups
Alveolar C-fibers
fire in response to lung injury,
overinflation, pulmonary edema, pulmonary embolism
not sensitive to inflammatory mediators
Bronchial C-fibers
are sensitive to inflammatory
mediators
Stimulation bronchial C fibers
rapid shallow breathing,
bronchoconstriction, airway secretion and cardiovascular
depression (i.e. hypotension and bradycardia)
Proprioceptors
Present in joints, tendons and muscle
inform brain of position of body through reception of tension
Patient without proprioception…
brain has no
information on the location of your extremities must watch their limbs
What is sobriety test testing?
proprioception
What happens during repeat inflammation in the lungs?
destruction of alveolar septa and lungs with large air sacs rather than small alveoli
leads to hypoxemia and dyspnea
Davenport Diagram
When respiratory acidosis occurs:
Renal Compensation through ‘Metabolic alkalosis’
Secrete H+into urine
blood pH↑
HCO3- ↑
CSF pH with chronic hypercapnia
Choroid plexus will restore CSF pH by secreting HCO3 into the CSF to compensate for chronic acidosis
Minute ventilation during oxygen
induced hypercapnia
high O2 administered, initial decrease in minute ventilation but then increases
hypercapnia continues to increase
Carbon dioxide retention
consequence of
ventilation-perfusion mismatching rather than respiratory
center depression
How can you reduce risk of oxygen-induced
hypercapnia in COPD patients?
titrate oxygen delivery to maintain the PaO2 at 60-65 mm Hg
achieve
saturations of 88% to 92%
Consequences of Hypoxaemia
Regional pulmonary vasoconstriction
Peripherally vasodilation increase Cardiac output
Erythropoietin secretion increases
Loss of cognitive and motor functions
Impaired judgement
headache,
breathlessness, palpitations, tremor ,
restlessness
loss of consciousness
Detrimental long term effects: pulmonary
HT, Right Ventricular failure, polycythaemia
Why treat Hyoxaemia?
Immediate benefits – Alleviate of hypoxaemia,
reduce dyspnea, sleep consolidation
Long term benefits – improves survival
-slight reduction in
pulmonary artery pressure
